Record 1 of 109 in AGRICOLA (1998-2001/09)
AN: IND 21237640
AU: Beshgetoor,-D.; Lonnerdal,-B.
TI: Effect of marginal maternal zinc deficiency in rats on mammary gland zinc metabolism.
SO: J-nutr-biochem. New York, N.Y. : Elsevier Science Inc. Oct 1997. v. 8 (10) p. 573-578.
CN: DNAL QP141.A1J54
IS: ISSN: 0955-2863
DE: maternal-nutrition. trace-element-deficiencies. mineral-metabolism. nutrient-transport. experimental-diets. nutrient-intake. nutrient-retention. copper-. iron-.
AB: There is a paucity of studies investigating the consequences of marginal zinc deficiency (MZD) during the reproductive cycle. This study was conducted to characterize the effects of MZD during pregnancy and lactation with a focus on zinc (Zn) transfer into the mammary gland and milk. Female Sprague-Dawley rats were fed a control diet (28 micrograms/g) or a marginally low Zn diet (12 micrograms/g) during pregnancy and lactation or the control diet during pregnancy followed by the low Zn diet during lactation. Pair-fed controls received the control diet in amounts adjusted to the mean daily intake of rats fed the low Zn diet. Pup weight and maternal mammary tissue weight were significantly lower in dams fed the MZD diet throughout pregnancy and lactation. Milk volume was significantly lower in both MZD groups. 65Zn tissue retention was higher in the liver of MZD dams in contrast to lower 65Zn in mammary tissue and milk. Iron and copper levels in dams and pups were not affected by dietary Zn. Although MZD during pregnancy and lactation did not impair maternal health, it significantly reduced mammary weight, milk volume and mammary Zn transfer, thus impairing factors important to neonatal growth.
Record 2 of 109 in AGRICOLA (1979 - 1984)
AN: FNI 81001286
TI: A new look at zinc.
SO: Prof-Nutr. San Francisco. Oct/Dec 1980. v. 12 (4) p. 4-6. ill.
AB: Abstract: Recent investigations into the role of zinc in human nutrition have shown that it is essential for normal growth and development, epithelial tissue function, reproduction, normal immune response, etc. The best sources of the required 15 mg. per day for adults are meats. Zinc is necessary for the enzymatic function of many metalloenzymes and in DNA and RNA. Zinc absorption is influenced by the presence of other nutrients; phytates, for example, reduce zinc bioavailability, and cow's milk proteins bind zinc. The liver seems to play an important processing role after absorption which helps maintain the plasma zinc balance and response to acute injury and chronic disease. Zinc may also be involved in stress response by influencing glucose metabolism. Clinical manifestations of zinc deficiency are rare, but include growth retardation, skin abnormalities, hypogonadism and acrodermatitis enteropathica. Zinc seems to be relatively non-toxic, but prolonged supplementation may induce copper deficiency.
Record 3 of 109 in AGRICOLA (1979 - 1984)
AN: IND 81000580
AU: Dinsdale,-D.; Williams,-R.B.
TI: Ultrastructural changes in the sperm tail of zinc-deficient rats.
SO: J-Comp-Pathol. London, Academic Press. Oct 1980. v. 90 (4) p. 559-566. ill.
CN: DNAL 41.8-J82
IS: ISSN: 0021-9975
Record 4 of 109 in AGRICOLA (1979 - 1984)
AN: FNI 79456509
TI: VA study ties zinc deficiency to male infertility.
SO: Med-World-News. New York, McGraw-Hill June 11, 1979. v. 20 (12) p. 12,16.
IS: ISSN: 0025-763X
DE: Zinc-. Fertility-. Males-. Deficiency-diseases-and-disorders. Weight-loss. Hormones-. Supplements-Nutrient. Minerals-. Vegetarians-.
AB: Abstract: Zinc deficiency has been linked with male sterility, according to a study of five middle-aged men following a zinc-restricted diet. The men underwent zinc depletion and their sperm counts dropped from a mean of 283 million/mL to 45 million within 2-14 months. Three of the men's sperm counts dropped to below 20 million, defined as sterility; the other two dropped below 60 million, considered oligospermic. Weight loss, lowered serum-testosterone levels and increased gonadotropic hormone levels were also experienced. Implications of the findings are: 1) oligospermia may suggest zinc deficiency; 2) unexplained oligospermia, if accompanied by low blood zinc level, may be treated with oral zinc; and 3) strict vegetarians may need zinc supplementation to become fertile, since zinc is mainly derived from animal protein.
Record 5 of 109 in AGRICOLA (1992-1997)
AN: IND 20580524
AU: Gilabert,-E.R.; Ruiz,-E.; Osorio,-C.; Ortega,-E.
TI: Effect of dietary zinc deficiency on reproductive function in male rats: biochemical and morphometric parameters.
SO: J-nutr-biochem. New York, N.Y. : Elsevier Science Inc. July 1996. v. 7 (7) p. 403-407.
CN: DNAL QP141.A1J54
IS: ISSN: 0955-2863
DE: zinc-. trace-element-deficiencies. reproductive-physiology. hcg-. gnrh-. body-weight. weight-gain. testes-. weight-. vesicular-gland. prostate-. seminiferous-tubules. alkaline-phosphatase. enzyme-activity. diet-. blood-serum. testosterone-. fsh-. lh-. biological-indicators. structure-. morphology-. rats-. male-animals.
AB: The effect of zinc on reproductive function was studied in rats fed with a zinc-deficient diet and control rats fed with a standard diet. Serum testosterone (T) levels were measured before and after the injection of HCG (human chorionic gonadotropin). Serum gonadotrophin levels were measured before and after the injection of GnRH (gonadotropin releasing hormone). In addition, structural parameters were studied and morphometric techniques were used to study the seminiferous tubules. The findings were used to investigate the possible relationship between biochemical and morphometric changes. Body weight (BW) gain, zinc content of testes and weight of the testes, seminal vesicle, and prostate were significantly lower in zinc-deficient rats compared with controls. Serum zinc concentrations and alkaline phosphatase activity were decreased in zinc-deficient rats compared with controls. Serum basal and stimulated FSH concentrations were similar in the two groups. Serum LH response to GnRH was higher in zinc-deficient rats. Serum basal T was lower in zinc deficient animals, but the response of T to HCG was similar in the two groups. The basal and luminal diameters, perimeter, and surface area of the seminiferous tubules as well as tubule volume, wall thickness, and cross-section area decreased in zinc-deficient animals in comparison with controls. Concentrations of zinc were significantly correlated with structural parameters and serum T levels. The changes in T levels correlated positively with the structural parameters and morphological findings.
Record 6 of 109 in AGRICOLA (1992-1997)
AN: IND 93045219
AU: Blamberg,-D.L.; Blackwood,-U.B.; Supplee,-W.C.; Combs,-G.F.
TI: Effect of zinc deficiency in hens on hatchability and embryonic development.
SO: Proc-Soc-Exp-Biol-Med. Baltimore, Md. : Williams & Wilkins. June 1960. v. 104 (2) p. 217-220.
CN: DNAL 442.9-SO1
IS: ISSN: 0037-9727
DE: pullets-. diet-. mineral-deficiencies. zinc-. reproductive-performance. embryonic-development. teratogenesis-. egg-hatchability.
Record 7 of 109 in AGRICOLA (1992-1997)
AN: FNI 92002719
AU: Hunt,-C.D.; Johnson,-P.E.; Herbel,-J.; Mullen,-L.K.
TI: Effects of dietary zinc depletion on seminal volume and zinc loss, serum testosterone concentrations, and sperm morphology in young men.
SO: Am-J-Clin-Nutr. Baltimore, Md. : American Society for Clinical Nutrition. July 1992. v. 56 (1) p. 148-157.
CN: DNAL-FNC 389.8-J824
IS: ISSN: 0002-9165
DE: zinc-. dietary-minerals. mineral-deficiencies. male-infertility. experimental-diets. depletion-. dosage-effects. mineral-content. semen-. spermatozoa-. testosterone-. blood-serum. ejaculation-. young-adults. men-.
AB: Identification of the andrological variables most sensitive to zinc depletion would expedite the diagnosis of male reproductive pathology, induced by zinc deficiency. Eleven volunteers living on a metabolic ward were fed a diet composed of a mixture of a semisynthetic formula and conventional foods, supplemented with ZnSO4 to supply a total of 1.4, 2.5, 3.4, 4.4, or 10.4 mg Zn/d. After an equilibration period of 28 d (10.4 mg Zn/d), all treatments were presented for 35 d each, the first four in random order and the fifth last. Compared with when they were consuming 10.4 mg Zn/d, volunteers consuming 1.4 mg Zn/d exhibited decreased semen volumes (3.30 vs 2.24 mL) and serum testosterone concentrations (26.9 vs 21.9 nmol/L), and no change in seminal zinc concentrations. Compared with 10.4 mg Zn/d, treatments of 1.4, 2.5, and 3.4 mg Zn/d decreased the total semen zinc loss per ejaculate (6.29 vs 3.81, 4.68, and 5.03 micromoles/ejaculate). Seminal loss accounted for 9% of total body zinc loss when 1.4 mg Zn/d was consumed. Seminal phosphorus concentrations were elevated during all four phases of zinc depletion (28.4 vs 32.9, 31.0, 34.2, and 33.6 mmol/L). The findings suggest that serum testosterone concentrations, seminal volume, and total seminal zinc loss per ejaculate are sensitive to short-term zinc depletion in young men.
Record 8 of 109 in AGRICOLA (1984 - 12/91)
AN: IND 90057638
AU: Hunt,-C.D.; Achen,-V.; Johnson,-P.E.
TI: Effects of short-term dietary zinc deficiency on sperm morphology and motility in humans.
SO: Proc-N-D-Acad-Sci. Grand Forks, N.D. : The Academy. Apr 1990. v. 44 p. 65.
CN: DNAL 500-N813
IS: ISSN: 0096-9214
DE: trace-element-deficiencies. zinc-. human-experimentation. morphology-. motility-. spermatozoa-.
Record 9 of 109 in AGRICOLA (1984 - 12/91)
AN: IND 89042076
TI: Effect of testosterone treatment on reproductive organ growth of Zn-deficient male rats.
SO: Proc-N-D-Acad-Sci. Grand Forks, N.D. : The Academy. Apr 1989. v. 43 p. 72.
CN: DNAL 500-N813
IS: ISSN: 0096-9214
DE: zinc-. deficiency-diseases. diet-studies. human-nutrition-research. rats-. reproductive-disorders. testosterone-. therapy-.
Record 10 of 109 in AGRICOLA (1984 - 12/91)
AN: FNI 87001138
AU: Barlow,-P.J.; Sidani,-S.; Rice,-R.D.; Barnes,-B.; Grant,-E.; Kingsley,-P.; Tatham,-P.; Mumby,-K.; Lester,-J.; Nichols,-J.
TI: Nutrition and pre-conception care.
SO: Lancet. Boston, Mass. : Little, Brown and Company. Dec 7, 1985. v. 2 (8467) p. 1297-1298.
CN: DNAL 448.8-L22
IS: ISSN: 0099-5355
DE: hair-analysis. zinc-. pregnant-women. mineral-deficiencies. food-and-nutrition-controversies.
AB: Abstract: A series of 4 letters to the editor provides criticisms and related information concerning a prior critical editorial on hair analysis, nutrition assessment, and preconception care for pregnant women. Particular criticism is given to the methodology and errors associated with hair analysis and its utility for assessing zinc nutritional status. It is argued that mineral hair analysis, properly done, can provide useful information on both zinc status and zinc deficiency in pregnant women and on possible exposures to toxic heavy metals.(wz).
Record 11 of 109 in AGRICOLA (1984 - 12/91)
AN: FNI 86010319
TI: Preconceptional and prenatal nutrition: Part II- Vitamins, minerals, alcohol, and caffeine.
SO: J-Can-Diet-Assoc. Toronto, Ont. : The Association. Summer 1985. v. 46 (3) p. 176-181. ill., charts.
CN: DNAL 389.9-C1632
IS: ISSN: 0008-3399
DE: maternal-nutrition. prenatal-period. nutrient-intake. vitamins-. minerals-. caffeine-. ethanol-. literature-reviews.
AB: Abstract: The importance of vitamins, minerals, alcohol, and caffeine to women and their infants before conception and during pregnancy is reviewed and discussed. While good knowledge of the development of birth defects by a mineral deficiency (iodine) or vitamin excesses (vitamin A and D) is available, the effects of vitamin and mineral excesses and deficiencies in general are not well understood. Recent data indicate that even small doses of alcohol may adversely effect the fetus. The effects of caffeine (especially, coffee) intake during pregnancy on fetal development remain unclear. Data on the effects of iron, calcium, and zinc are reviewed. (wz).
Record 12 of 109 in AGRICOLA (1984 - 12/91)
AN: FNI 84004152
AU: Wynn,-Margaret.; Wynn,-Arthur.
CA: Nourishment for the Next Generation: from Preconception to Weaning-the Influence of Nutrition (1982 July : Oxford, England).
TI: Effects of nutrition on reproductive capability.
SO: Nutr-Health. Berkhamstead : A B Academic Publishers. 1983. v. 1 (3/4) p. 165-178. ill., charts.
CN: DNAL RC620.A1N84
IS: ISSN: 0260-1060
AB: Abstract: Nutritional status can impact reproductive capability. The endocrine system is sensitive to the consequences of malnutrition as is the hypothalamus (malnutrition produces hormone secretions affecting fertility in both sexes and prohibiting growth and lactaction. Pituitary, liver, and ovarian hormone secretions are inhibited by nutritional inadequacies. Caloric restrictions inhibit the hypothalamic-pituitary system as do deficiencies of pyridoxine, folic acid, zinc, and magnesium. Maternal malnutrition prior to conception has a greater impact on the embryo than malnutrition during the last 2 trimesters. (kbc).
Record 13 of 109 in SilverPlatter MEDLINE(R) (2001/01-2001/10)
TI: Increased apoptosis in a variety of tissues of zinc-deficient rats.
AU: Nodera,-M; Yanagisawa,-H; Wada,-O
SO: Life-Sci. 2001 Aug 24; 69(14): 1639-49
AB: Zinc deficient rats were prepared to investigate histopathological changes in thymus, testis, skin, esophagus, kidney and liver and the relationship between these changes and apoptosis. Seven-week-old male SD rats were given a Zn deficient diet (0% Zn diet) or a standard diet (0.02% Zn diet). The above-mentioned organs were excised 1, 2, 3, 4, 5, 10, 13, and 34 weeks after initiating diet administration. Then, these organs were examined morphologically, and apoptotic changes were analyzed by either the TdT- mediated dUTP - biotin nick end labeling (TUNEL) or electrophoresis. Significant morphological changes were seen only in rats on the 0% Zn diet. After 4 weeks, atrophy of the thymus was seen. After 5 weeks, oligospemia was observed, and after 10 weeks, testicular atrophy accompanied by the loss of sperm cells and spermatocytes was confirmed. In addition, after 10 weeks, thickening of epithelia was seen in the skin and esophagus of rats on the 0% diet. During the observation period, no marked morphological changes were observed in the liver or kidney. In the thymus and testis of rats on the 0% Zn diet, prior to detecting any morphological changes, increases in apoptosis were confirmed at 1 and 3 weeks after initiating diet administration, respectively. In the kidney and liver, TUNEL positive cells appeared after 13 and 34 weeks, respectively. These observations suggest that the functional and morphological changes in the thymus and testis of rats on the 0% Zn diet are caused by increased apoptosis, and that even when the supply of Zn is terminated for only a short period of time, immunocytes and germ cells can not survive or regenerate sufficiently. Again, the fact that even in the liver and kidney, apoptosis was observed when administration of the 0% Zn diet was prolonged suggests that the appearance of apoptosis is dependent on the amount of Zn in tissues. In addition, the fact that increases in apoptosis were confirmed in the skin of rats on the 0% Zn diet, but not in the esophagus of these rats suggests that apoptosis does not directly cause thickening of stratified squamous epithelium in Zn deficient rats.
Record 14 of 109 in SilverPlatter MEDLINE(R) (2001/01-2001/10)
TI: Zinc and the immune system.
AU: Rink,-L; Gabriel,-P
SO: Proc-Nutr-Soc. 2000 Nov; 59(4): 541-52
AB: Zn is an essential trace element for all organisms. In human subjects body growth and development is strictly dependent on Zn. The nervous, reproductive and immune systems are particularly influenced by Zn deficiency, as well as by increased levels of Zn. The relationship between Zn and the immune system is complex, since there are four different types of influence associated with Zn. (1) The dietary intake and the resorption of Zn depends on the composition of the diet and also on age and disease status. (2) Zn is a cofactor in more than 300 enzymes influencing various organ functions having a secondary effect on the immune system. (3) Direct effects of Zn on the production, maturation and function of leucocytes. (4) Zn influences the function of immunostimulants used in the experimental systems. Here we summarize all four types of influence on the immune function. Nutritional aspects of Zn, the physiology of Zn, the influence of Zn on enzymes and cellular functions, direct effects of Zn on leucocytes at the cellular and molecular level, Zn-altered function of immunostimulants and the therapeutic use of Zn will be discussed in detail.
Record 15 of 109 in SilverPlatter MEDLINE(R) (2001/01-2001/10)
TI: Prevalence of micronutrient deficiency particularly of iron, zinc and folic acid in pregnant women in South East Asia.
SO: Br-J-Nutr. 2001 May; 85 Suppl 2: S87-92
AB: Micronutrient deficiency, whether clinical or subclinical, may affect growth, cognition and reproductive performance. In pregnant women moderate to severe deficiencies of iron, zinc and folic acid have been shown to increase risk of low birth weight, pregnancy complications and birth defects. Any attempt to introduce a micronutrient supplementation programme during pregnancy must be based on adequate data on the prevalence of micronutrient deficiencies, their adverse effects and the potential for reversing these through supplementation. This paper reviews parameters for assessment of iron, zinc and folic acid deficiencies in pregnancy and the available data on prevalence of these in pregnant women in South Asia. Iron deficiency and anemia affect 50 % or more of pregnant women, the prevalence of folic acid deficiency may be up to 30-50 % and there is evidence to suggest that zinc deficiency is likely to be widespread but supportive data are scarce.
Record 16 of 109 in MEDLINE(R)+ (1998-2000)
TI: Male factor subfertility: possible causes and the impact of nutritional factors.
AU: Wong,-W-Y; Thomas,-C-M; Merkus,-J-M; Zielhuis,-G-A; Steegers-Theunissen,-R-P
SO: Fertil-Steril. 2000 Mar; 73(3): 435-42
AB: OBJECTIVE: To review possible causes for male factor subfertility with emphasis on nutritional factors such as zinc and folate. DESIGN: A literature search was performed on MEDLINE and via bibliographies of published works. RESULT(s): Many causes for male factor subfertility are described in the literature. Both environmental and genetic factors could play a role. However, the pathogenesis of male factor infertility is poorly understood, including the role of specific micronutrients such as zinc and folate. Both zinc and folate are involved in the synthesis of DNA and RNA. Despite the fact that zinc deficiency leads to several clinical symptoms such as decreased spermatogenesis and impaired male fertility, the exact pathophysiology has not been clarified. CONCLUSION(s): Because most causes of male factor subfertility are unknown, more research is needed. Because male factor subfertility due to nutritional deficiencies is in principle amenable to curative and/or preventive action by supplementation, emphasis should be put on studies on the effect of specific nutrients on male fertility.
Record 17 of 109 in MEDLINE(R)+ (1998-2000)
TI: Neurobiology of zinc-influenced eating behavior.
AU: Shay,-N-F; Mangian,-H-F
SO: J-Nutr. 2000 May; 130(5S Suppl): 1493S-9S
AB: Zinc is an essential nutrient that is required in humans and animals for many physiological functions, including immune and antioxidant function, growth and reproduction. Many aspects of zinc deficiency-induced anorexia have been well studied in experimental animals, most notably the laboratory rat. There is evidence that suggests zinc deficiency may be intimately involved with anorexia in humans: if not as an initiating cause, then as an accelerating or exacerbating factor that may deepen the pathology of the anorexia. The present review describes recent research investigating the relationship between zinc deficiency and the regulation of food intake, along with advances in the understanding of the food intake and body weight regulation systems. For more comprehensive reviews of zinc nutrition and zinc deficiency, readers are referred to the other reviews in this volume and the review text of Mills (1989). An excellent review focused solely on zinc status and food intake has been presented by O'Dell and Reeves (1989).
Record 18 of 109 in MEDLINE(R)+ (1998-2000)
TI: Functional compensation by Egr4 in Egr1-dependent luteinizing hormone regulation and Leydig cell steroidogenesis.
AU: Tourtellotte,-W-G; Nagarajan,-R; Bartke,-A; Milbrandt,-J
SO: Mol-Cell-Biol. 2000 Jul; 20(14): 5261-8
AB: The Egr family of zinc finger transcription factors, whose members are encoded by Egr1 (NGFI-A), Egr2 (Krox20), Egr3, and Egr4 (NGFI-C) regulate critical genetic programs involved in cellular growth, differentiation, and function. Egr1 regulates luteinizing hormone beta subunit (LHbeta) gene expression in the pituitary gland. Due to decreased levels of LHbeta, female Egr1-deficient mice are anovulatory, have low levels of progesterone, and are infertile. By contrast, male mutant mice show no identifiable defects in spermatogenesis, testosterone synthesis, or fertility. Here, we have shown that serum LH levels in male Egr1-deficient mice are adequate for maintenance of Leydig cell steroidogenesis and fertility because of partial functional redundancy with the closely related transcription factor Egr4. Egr4-Egr1 double mutant male mice had low steady-state levels of serum LH, physiologically low serum levels of testosterone, and atrophy of androgen-dependent organs that were not present in either Egr1- or Egr4-deficient males. In double mutant male mice, atrophic androgen-dependent organs and Leydig cell steroidogenesis were fully restored by administration of exogenous testosterone or human chorionic gonadotropin (an LH receptor agonist), respectively. Moreover, a normal distribution of gonadotropin-releasing hormone-containing neurons and normal innervation of the median eminence in the hypothalamus, as well as decreased levels of LH gene expression in Egr4-Egr1-relative to Egr1-deficient male mice, indicates a defect of LH regulation in pituitary gonadotropes. These results elucidate a novel level of redundancy between Egr4 and Egr1 in regulating LH production in male mice.
CN: CA4971210CANCI; MH142602MHNIMH
Record 19 of 109 in MEDLINE(R)+ (1998-2000)
TI: The effect of a zinc, cobalt and selenium soluble glass bolus on trace element status and semen quality of ram lambs.
AU: Kendall,-N-R; McMullen,-S; Green,-A; Rodway,-R-G
SO: Anim-Reprod-Sci. 2000 Sep 1; 62(4): 277-83
AB: Supplemental zinc and selenium were administered to ram lambs grazed on pastures that were not considered to be deficient in either element. The breeding season and polygamy of the ram mean that his requirements for semen production will be relatively large over a short breeding season and this may induce a localised deficiency of zinc and/or selenium, thus resulting in a decrease in semen quality and production.Thirty-three 8-month-old ram lambs were kept at grass and fed a supplement of barley and peas, with ad libitum access to grass silage when grazing became restricted. On day 0, the rams were allocated to two groups by restricted randomisation of live weight. One group each had a zinc, cobalt and selenium soluble glass bolus (Zincosel(R), Telsol) administered with the other group not receiving a bolus to act as a control. Blood samples were taken by jugular venipuncture at day 0 (prior to bolus administration) and at days 23, 44, 65 and 86. Blood samples were analysed for zinc status (plasma zinc concentration) and selenium status (erythrocyte glutathione peroxidase activity). Semen was collected once a week between days 44 and 86, by diversion during a natural mount. Semen quality was assessed by ejaculate volume, spermatocrit, sperm concentration, abnormal morphology, motility, percentage live (negrosin-eosin stain), membrane integrity (hypo-osmotic swelling test (HOS)) and seminal fluid glutathione peroxidase activity and zinc concentration. The bolused lambs had a significantly increased erythrocyte glutathione peroxidase activity (P<0.01) on all samplings after bolusing and had significant increases in motility, proportion of live sperm and proportion of intact membranes indicated by the HOS. The bolused ram lambs had an increased selenium status and apparent improvement in semen membrane quality.
Record 20 of 109 in MEDLINE(R)+ (1998-2000)
TI: Testicular atrophy, zinc concentration, and angiotensin-converting enzyme activity in the testes of vitamin A-deficient rats.
AU: Rahman,-A-S; Kimura,-M; Itokawa,-Y
SO: Biol-Trace-Elem-Res. 1999 Jan; 67(1): 29-36
AB: Angiotensin-converting enzyme (ACE) as a part of the renin angiotensin system (RES) regulates blood pressure and fluid and electrolyte homeostasis, and the enzyme is considered to have a function in reproduction. Reduced enzyme activities have been observed in atrophied testes as a results of zinc and pituitary deficiencies. Vitamin A deficiency causes atrophy of testes. The present study was conducted on three groups of male, 3-wk-old, Wistar rats. After 54 d of the experimental period, testicular weights of the vitamin A-deficient rats (A- group, allowed free access to vitamin A- deficient diet) was significantly lower than its pair-fed, PF (given restricted amount control diet) and A+ (allowed free access to control diet) groups. Zinc concentrations and both soluble and particulate ACE activities in the testes of vitamin A- deficient rats (A- group) were significantly lower than the other two groups. No significant differences were observed regarding zinc concentration, particulate ACE, and total ACE activities in the testes of PF and A+ groups. Vitamin A deficiency did not significantly affect the enzyme activity in the lung. From the observations of the present study, we speculate that testicular atrophy in vitamin A deficiency may have resulted from lower zinc concentration and decreased ACE activity in that organ.
Record 21 of 109 in MEDLINE(R)+ (1998-2000)
TI: Maternal trace elements, vitamin B12, vitamin A, folic acid, and fetal malformations.
AU: Stoll,-C; Dott,-B; Alembik,-Y; Koehl,-C
SO: Reprod-Toxicol. 1999 Jan-Feb; 13(1): 53-7
AB: The demonstrated teratogenicity of maternal zinc deficiency in rats has led to burgeoning interest in zinc and other trace elements as important factors in embryonic development. Levels of zinc, copper, manganese, magnesium, folic acid, vitamin B12 and vitamin A were evaluated at the beginning of pregnancy in the plasma of pregnant women who later delivered a malformed newborn. Fetal chromosomal anomalies and recognizable nonchromosomal syndromes were excluded. The results were compared to control women who delivered normal babies. One hundred seventy mothers had malformed children. The more frequent congenital malformations were congenital heart diseases (72 cases including 24 VSD), musculoskeletal malformations (21 cases), urogenital malformations (23 cases), spina bifida (6 cases), hydrocephaly (6 cases), and labial cleft (14 cases). Maternal plasma concentrations of zinc, copper, magnesium, manganese, folate, vitamin B12, and vitamin A of malformed children did not differ from controls. Thus vitamin profiles do not form a suitable means for identifying women at risk for having a child with congenital malformations.
Record 22 of 109 in MEDLINE(R)+ (1998-2000)
TI: Numerical dose-compensated in vitro fertilization inseminations yield high fertilization and pregnancy rates.
AU: Benoff,-S; Cooper,-G-W; Paine,-T; Hurley,-I-R; Napolitano,-B; Jacob,-A; Scholl,-G-M; Hershlag,-A
SO: Fertil-Steril. 1999 Jun; 71(6): 1019-28
AB: OBJECTIVE: To evaluate in cases with morphologically abnormal sperm whether fertilization and pregnancy rates are increased by normalizing the number of sperm inseminated and whether biomarkers can identify cases of reduced or failed fertilization. DESIGN: Prospective studies of sperm morphology and function. SETTING: University hospital assisted human reproduction program. PATIENT(S): Partners of 308 women undergoing IVF. INTERVENTION(S): Motile sperm populations were assessed for sperm head morphology, for surface receptors for mannose and progesterone binding, and the ability to undergo a free mannose-induced acrosome reaction. Zinc in seminal plasma was determined by atomic absorption spectroscopy. MAIN OUTCOME MEASURE(S): Sperm morphology was associated with fertilization and clinical pregnancy rates. Biomarker analyses were correlated with fertilization rates using Kruskal-Wallis tests, chi2 tests, and Spearman rank order correlations. RESULT(S): Fertilization and pregnancy rates after numerical dose compensation inseminations were indistinguishable between men with differing percentages of normal sperm. Biomarker deficits were identified irrespective of sperm head morphology in 96% of cases of reduced or failed fertilization. CONCLUSION(S): Fertilization and pregnancy rates in cases of abnormal morphology are optimized by inseminating at least 25,000 sperm/mL with normal acrosomes. Reduced or failed fertilization can be predicted by testing for molecular deficits in mannose receptor expression and mannose-stimulated acrosome loss.
Record 23 of 109 in MEDLINE(R)+ (1998-2000)
TI: Plasma vitamin A, E, and beta-carotene levels in adult post-partum Algerian women.
AU: Lachili,-B; Faure,-H; Smail,-A; Zama,-N; Benlatreche,-C; Favier,-A; Roussel,-A-M
SO: Int-J-Vitam-Nutr-Res. 1999 Jul; 69(4): 239-42
AB: Vitamins A and E are essential for foetal growth, reproduction, and lactation. In this article we report the results of a study, lead in three Eastern Algeria cities, that involved 786 post-partum women and 250 control. Plasma levels of vitamins A, E, beta-carotene, and some nutritional indexes were measured in both groups. In control women, plasma retinol and beta-carotene levels were significantly lower in Algeria than in France (retinol: 1.4 +/- 0.42 vs. 1.78 +/- 0.53 mumol/l; beta-carotene: 0.35 +/- 0.261 vs. 0.94 +/- 0.611). These differences could be the consequence of different beta-carotene and retinol intakes. In Algeria, comparisons between post-partum women and controls, showed that plasma vitamin A and beta-carotene levels were significantly lower in post-partum than in control women. This fact, and the lower level of retinol in control women, raises the question of supplementation for pregnant women in Algeria, at least for those with the lowest standard of living whose protein and zinc levels are also very low after delivery. Plasma vitamin E levels and vitamin E/total lipid ratios were not different in Algeria and in France. Vitamin E concentration was higher during pregnancy, but the vitamin E/total lipid ratio was significantly lower, which shows a relative deficiency at the end of pregnancy. Comparisons of plasma vitamin E levels, at delivery, in primiparous and in multiparous women reveal a better tocopherol status in multiparous women. This difference could reflect an adaptive response to oxidative stress in multiparous women.
Record 24 of 109 in MEDLINE(R)+ (1998-2000)
TI: Chronic cadmium toxicity to sperm of heavy cigarette smokers: immunomodulation by zinc.
AU: Al-Bader,-A; Omu,-A-E; Dashti,-H
SO: Arch-Androl. 1999 Sep-Oct; 43(2): 135-40
AB: The aim of the study was to investigate the role of zinc therapy in 125 male cigarette smokers with infertility. The mechanism involved in the zinc/cadmium relationship was evaluated through the effect of a zinc-deficient diet and supplementation on testes of male adult Sprague-Drew rats. Heavy smoking was associated with low sperm count, motility, and morphology and increased seminal cadmium levels. Zinc therapy improved sperm quality and increased seminal IL-4, but reduced TNF-alpha and IFN-gamma. A zinc-deficient diet led to high cadmium testicular accumulation comparable with those supplemented with cadmium. Cadmium had a linear correlation with TNF-alpha and IFN-gamma, but not with IL-4. Cytology of testicular aspirate and histopathology were normal in supplemented groups as in controls. These results indicate that zinc modulates the putative effect of cadmium through its enhancement of T-helper 2 cytokines expression and down-regulation of T-helper 1 cytokines.
Record 25 of 109 in MEDLINE(R)+ (1998-2000)
TI: Infertility associated with incomplete spermatogenic arrest and oligozoospermia in Egr4-deficient mice.
AU: Tourtellotte,-W-G; Nagarajan,-R; Auyeung,-A; Mueller,-C; Milbrandt,-J
SO: Development. 1999 Nov; 126(22): 5061-71
AB: Male fertility is complex and depends upon endocrine/paracrine regulatory mechanisms and morphogenetic processes occurring during testicular development, spermatogenesis (mitosis and meiosis) and spermiogenesis (spermatid maturation). Egr4 (NGFI-C, pAT133), a member of the Egr family of zinc-finger transcription factors, is thought to be involved in cellular growth and differentiation, but its specific function has been previously unknown. We derived Egr4 null mice through targeted mutagenesis and found that they were phenotypically normal with the exception that males, but not females, were infertile. Egr4 is expressed at low levels within male germ cells during meiosis and is critical for germ cell maturation during the early-mid pachytene stage. While most Egr4 null male germ cells undergo apoptosis during early-mid pachytene, some are capable of maturing beyond an apparent Egr4-dependent developmental restriction point. Consequently, a limited degree of spermiogenesis occurs but this is accompanied by markedly abnormal spermatozoon morphology and severe oligozoospermia. Egr4 appears to regulate critical genes involved in early stages of meiosis and has a singularly important role in male murine fertility. These data raise the possibility that Egr4 may contribute to some forms of human idiopathic male infertility.
CN: 5K08MH142602MHNIMH; 5P01CA4971208CANCI
Record 26 of 109 in MEDLINE(R)+ (1998-2000)
TI: Developmental and physiologic roles of the nuclear receptor steroidogenic factor-1 in the reproductive system.
AU: Sadovsky,-Y; Crawford,-P-A
SO: J-Soc-Gynecol-Investig. 1998 Jan-Feb; 5(1): 6-12
AB: OBJECTIVE: To characterize the unique features of steroidogenic factor-1 (SF-1) among members of the steroid receptor superfamily of proteins and review its role in reproductive development and function. METHODS: We reviewed all pertinent articles that describe structural or functional aspects of SF-1. We also introduced results obtained recently by our group. RESULTS: Unlike other steroid receptors, SF-1 binds as a monomer to a DNA response element, which is composed of an estrogen receptor "half site." Furthermore, SF-1 lacks a specific ligand that is required for either interaction with DNA or modulation of its transactivation function. Steroidogenic factor-1 is highly expressed in steroid-producing tissues and in gonadotrophs and plays a pivotal role in regulating the expression of enzymes and hormones essential for steroid biosynthesis pathways. A dramatic phenotype was revealed using SF-1 deficient mice: these mice lack gonads and adrenal glands, establishing SF-1 as an essential embryonic regulator of steroidogenic organ development. While SF-1 is required for basal expression of steroidogenic enzymes, its role in hormone-dependent regulation of reproductive function in vivo is uncertain, but its function may be subject to modulation by coactivators or corepressors and hormones, as well as by post-translational modifications. CONCLUSION: Steroidogenic factor-1 plays a key role in the development and differentiation of the reproductive system. Understanding the mechanism of action of SF-1 is expected to provide new clues to the etiology of maldevelopment of the gonads and adrenal glands, and to dysfunction associated with steroid biosynthesis during early embryonic development and throughout differentiation.
Record 27 of 109 in MEDLINE(R)+ (1998-2000)
TI: Reduced fertility in female mice lacking copper-zinc superoxide dismutase.
AU: Ho,-Y-S; Gargano,-M; Cao,-J; Bronson,-R-T; Heimler,-I; Hutz,-R-J
SO: J-Biol-Chem. 1998 Mar 27; 273(13): 7765-9
AB: Copper-zinc superoxide dismutase (CuZn-SOD) is believed to play a major role in the first line of antioxidant defense by catalyzing the dismutation of superoxide anion radicals to form hydrogen peroxide and molecular oxygen. Recent studies have shown that missense mutations in this gene contribute, evidently through a gain-of-function mechanism, to about 20% of familial amyotrophic lateral sclerosis. To define further the physiologic role of this enzyme, a model of mice deficient in this enzyme was generated using gene targeting technology. Mice lacking this enzyme were apparently healthy and displayed no increased sensitivity to hyperoxia. However, they exhibited a pronounced susceptibility to paraquat toxicity. Most surprisingly, female homozygous knock-out mice showed a markedly reduced fertility compared with that of wild-type and heterozygous knock-out mice. Further studies revealed that although these mice ovulated and conceived normally, they exhibited a marked increase in embryonic lethality. These data, for the first time, suggest a role of oxygen free radicals in causing abnormality of female reproduction in mammals.
CN: ES06807ESNIEHS; HL56421HLNHLBI; P30ES06639ESNIEHS
Record 28 of 109 in MEDLINE(R)+ (1998-2000)
TI: Suboptimal zinc status in pregnant Malawian women: its association with low intakes of poorly available zinc, frequent reproductive cycling, and malaria.
AU: Gibson,-R-S; Huddle,-J-M
SO: Am-J-Clin-Nutr. 1998 Apr; 67(4): 702-9
AB: A study of 152 rural Malawian women aged 23.2+/-5.5 y (x+/-SD) at 24 wk gestation included measurements of biochemical indexes of zinc (plasma and hair), protein (serum albumin), and infection (serum C-reactive protein, white blood cell count, and malaria), and dietary intakes (via three interactive 24-h dietary recalls). Data on health, demographic and socioeconomic status, family characteristics, reproductive history, and anthropometry were also collected. The study revealed a high prevalence of suboptimal zinc status: 36% of the women had low plasma and 46% had low hair zinc values. Median daily intake of zinc (9.0 mg) was low and poorly available: 61% was provided by cereals and 20% by flesh foods. Median intake of animal protein was only 5.6 g/d, and phytate intakes were high (1.4 g/d). Women consuming diets with phytate-zinc ratios > 17 (the median) had lower hair zinc concentrations (1.6 compared with 1.8 micromol/g, P < 0.03), were older (24 compared with 20 y, P < 0.02), and had a higher number of pregnancies (3 compared with 2, P < 0.02) than those consuming diets with a phytate-zinc ratio < 17. Frequent reproductive cycling was related to zinc status; hair zinc was higher for a prima- than for a multigravida (2.0 compared with 1.6 micromol/g, P < 0.01). Malaria prevalence was also associated with hair zinc (P < 0.05) but not with plasma zinc, after the number of pregnancies was controlled for. We conclude that low intakes of poorly available dietary zinc, frequent reproductive cycling, and malaria prevalence are three major factors in the etiology of suboptimal zinc status in these rural, pregnant Malawian women.
Record 29 of 109 in MEDLINE(R)+ (1998-2000)
TI: Ovarian function in superoxide dismutase 1 and 2 knockout mice.
AU: Matzuk,-M-M; Dionne,-L; Guo,-Q; Kumar,-T-R; Lebovitz,-R-M
SO: Endocrinology. 1998 Sep; 139(9): 4008-11
AB: Copper/zinc superoxide dismutase (SOD1) and manganese superoxide dismutase (SOD2) are the two major intracellular enzymes which inactivate superoxide radicals. SOD1 is present in both cytoplasmic and nuclear compartments whereas SOD2 is localized to mitochondria. Both enzymes are expressed in multiple tissues as well as ovaries of several species including humans and rodents. Dominant mutations in SOD1 are associated with amyotrophic lateral sclerosis. We have previously demonstrated that SOD2-deficient mice die within three weeks of birth due to oxidative mitochondrial injury in central nervous system neurons and cardiac myocytes. In this report, we demonstrate that female homozygous mutant mice lacking SOD1 can survive to the adult stage but are subfertile. Whereas breeding of 5 SOD1 heterozygote females produced an average of 1.0 litter/month with 8.6 offspring/litter (n = 31 litters), only 11 of 16 SOD1 homozygote mice over a 2-6 month period became pregnant averaging 0.23 litters/month with an average litter size of 2.7 (n = 21 litters). Histological analysis of the ovaries from SOD1-deficient mice often reveals many primary and small antral follicles but few corpora lutea. In addition, ovaries from postnatal SOD2-deficient mice, transplanted to the bursa of wild-type hosts, show all stages of folliculogenesis including corpora lutea and can give rise to viable offspring. These studies support an important role of SOD1 in female reproductive function and suggest that SOD2 is not essential for ovarian function.
Record 30 of 109 in MEDLINE(R)+ (1998-2000)
TI: The role of copper, molybdenum, selenium, and zinc in nutrition and health.
AU: Chan,-S; Gerson,-B; Subramaniam,-S
SO: Clin-Lab-Med. 1998 Dec; 18(4): 673-85
AB: Copper, zinc, selenium, and molybdenum are involved in many biochemical processes supporting life. The most important of these processes are cellular respiration, cellular utilization of oxygen, DNA and RNA reproduction, maintenance of cell membrane integrity, and sequestration of free radicals. Copper, zinc, and selenium are involved in destruction of free radicals through cascading enzyme systems. Superoxide radicals are reduced to hydrogen peroxide by superoxide dismutases in the presence of copper and zinc cofactors. Hydrogen peroxide is then reduced to water by the selenium-glutathione peroxidase couple. Efficient removal of these superoxide free radicals maintains the integrity of membranes, reduces the risk of cancer, and slows the aging process. On the other hand, excess intake of these trace elements leads to disease and toxicity; therefore, a fine balance is essential for health. Trace element--deficient patients usually present with common symptoms such as malaise, loss of appetite, anemia, infection, skin lesions, and low-grade neuropathy, thus complicating the diagnosis. Symptoms for intoxication by trace elements are general, for example, flu-like and CNS symptoms, fever, coughing, nausea, vomiting, diarrhea, anemia, and neuropathy. A combination of observation, medical and dietary history, and analyses for multiple trace elements is needed to pinpoint the trace element(s) involved. Serum, plasma, and erythrocytes may be used for the evaluation of copper and zinc status, whereas only serum or plasma is recommended for selenium. Whole blood is preferred for molybdenum. When trace element levels are inconsistent with medical evaluations, a test for activity of the suspected enzyme(s) would support the differential diagnosis. Furthermore, it is important to differentiate whether trace element deficiency or toxicity is the primary cause of the disorder, or is secondary to other underlying diseases. Only successful treatment of the primary disorder will lead to complete recovery. In the event of sample contamination during collection or analysis, the physician may be misled by falsely elevated results. Royal blue top evacuated tubes containing negligibly low concentrations of the trace element or acid-washed plastic sterilized syringes should be used for blood, serum, or plasma collection. Powdered gloves must be avoided. When possible, mineral supplements are not to be administered to the patient for a minimum of 3 days prior to sample collection. Serum and plasma specimens are to be transported in acid-washed polypropylene and polyethylene tubes. Analysis is performed in a controlled environment to minimize or eliminate contamination. During analysis, all laboratory wares should be acid-washed for decontamination. A detailed description of these precautions may be found in reviews by Aitio and Jarvisalo and by Chan and Gerson. Copper and zinc analysis on serum and plasma are commonly performed by flame atomic absorption spectrometry, inductively coupled plasma-atomic emission spectrometry, and inductively coupled plasma-mass spectrometry. Serum and plasma selenium levels are determined by graphite furnace atomic absorption with Zeeman background correction and neutron activation analysis. Molybdenum levels are best determined by neutron activation and highly sensitive inductively coupled plasma-mass spectrometry. The reader is referred to reviews by Tsalev and Jarvis.
Record 31 of 109 in MEDLINE(R)+ (1998-2000)
TI: The molecular basis for the role of zinc in developmental biology.
SO: Mol-Cell-Biochem. 1998 Nov; 188(1-2): 41-8
AB: Zinc regulates the gene expression machinery. It affects the structure of chromatin, the template function of its DNA, the activity of numerous transcription factors and of RNA polymerases. Hence, it determines both the types of mRNA transcripts synthesized and the rate of transcription itself. Alterations in one or more of these zinc dependent processes have been proposed to account for the proliferative arrest and teratology induced by zinc deficiency. To examine this proposal, studies of zinc during X. laevis development have been initiated. The kinetics of X. laevis oocyte zinc uptake and storage and of zinc utilization during embryogenesis have been examined first. Vitellogenin carries zinc into the oocyte. Ten % of the total zinc (10 ng/egg) remains within the cytosol while 90% (90 ng/egg) is stored in the yolk platelets associated with lipovitellin. The cytosolic pool is the source of the zinc for all newly formed metalloproteins involved in embryo development. The yolk platelet zinc pool is stored for later use during early metamorphosis. It is now possible to examine zinc transfer to molecules, such as e.g. transcription factors, and the role of the metal in their function in development and organogenesis.
Record 32 of 109 in MEDLINE(R)+ (1995-1997)
TI: A potential role for cadmium in the etiology of varicocele-associated infertility.
AU: Benoff,-S; Hurley,-I-R; Barcia,-M; Mandel,-F-S; Cooper,-G-W; Hershlag,-A
SO: Fertil-Steril. 1997 Feb; 67(2): 336-47
AB: OBJECTIVE: To determine whether mannose ligand receptor and acrosome reaction deficits in sperm from men with varicocele are related to the transition metal content of their semen. DESIGN: Cadmium and zinc in semen and blood plasma were assayed for fertile males, men without varicocele who required intracytoplasmic sperm injection to achieve fertilization, and men evaluated for potential varicocele-associated infertility. The relationship between actin cytoskeletal distributions and acrosome status was determined for fertile donor sperm in the presence and absence of exogenous cadmium. SETTING: University hospital-based molecular biology research laboratory. PATIENT(S): Patients from two university hospital-based IVF-assisted reproductive technology programs and two male urology private practices. INTERVENTION(S): Fertile donor sperm were exposed to exogenous cadmium during capacitating incubations followed by culture at temperatures up to 41 degrees C. MAIN OUTCOME MEASURE(S): Metal ion levels in semen and blood plasma were determined by graphite furnace atomic absorption spectroscopy. Motile sperm were examined for mannose ligand binding and the ability to undergo spontaneous and induced acrosome reactions. Unfixed, Triton-permeabilized sperm were probed with antiactin and antimyosin antibodies. RESULT(S): Cadmium was elevated and zinc was decreased in the seminal plasma of men with varicocele. The content of these metals in semen and blood was not correlated. Cadmium exposure in vitro reduced mannose receptor expression, acrosome exocytosis, and cytoskeletal formation by fertile donor sperm. CONCLUSION(S): Defects in transition metal regulation or excessive cadmium exposure are involved in varicocele-associated infertility.
Record 33 of 109 in MEDLINE(R)+ (1995-1997)
TI: Zfx mutation results in small animal size and reduced germ cell number in male and female mice.
AU: Luoh,-S-W; Bain,-P-A; Polakiewicz,-R-D; Goodheart,-M-L; Gardner,-H; Jaenisch,-R; Page,-D-C
SO: Development. 1997 Jun; 124(11): 2275-84
AB: The zinc-finger proteins ZFX and ZFY, encoded by genes on the mammalian X and Y chromosomes, have been speculated to function in sex differentiation, spermatogenesis, and Turner syndrome. We derived Zfx mutant mice by targeted mutagenesis. Mutant mice (both males and females) were smaller, less viable, and had fewer germ cells than wild-type mice, features also found in human females with an XO karyotype (Turner syndrome). Mutant XY animals were fully masculinized, with testes and male genitalia, and were fertile, but sperm counts were reduced by one half. Homozygous mutant XX animals were fully feminized, with ovaries and female genitalia, but showed a shortage of oocytes resulting in diminished fertility and shortened reproductive lifespan, as in premature ovarian failure in humans. The number of primordial germ cells was reduced in both XX and XY mutant animals at embryonic day 11.5, prior to gonadal sex differentiation. Zfx mutant animals exhibited a growth deficit evident at embryonic day 12.5, which persisted throughout postnatal life and was not complemented by the Zfy genes. These phenotypes provide the first direct evidence for a role of Zfx in growth and reproductive development.
Record 34 of 109 in MEDLINE(R)+ (1995-1997)
TI: Effect of marginal or severe dietary zinc deficiency on testicular development and functions of the rat.
AU: Hamdi,-S-A; Nassif,-O-I; Ardawi,-M-S
SO: Arch-Androl. 1997 May-Jun; 38(3): 243-53
AB: The effects of marginal (MZD) and severe (SZD) zinc-deficient diets on testicular function and development were studied in rats maintained on dietary treatment for 6 weeks after weaning. SZD produced variable degrees of histological changes as compared with pair-fed controls, including a significant decrease in the diameter of seminiferous tubules (p < .05) with variable degree of maturation arrest in different stages of spermatogenesis. No significant histological changes were obtained in testes of MZD rats. MZD rats-exhibited significant decreases in serum levels of testosterone (62.6%, p < .001) and progesterone (18.2%, p < .05) with no changes in that of FSH or LH. SZD rats showed marked decreases in serum levels of testosterone (17.8-fold, p < .001) and progesterone (28.8%, p < .001), whereas FSH showed an increase (34.4%, p < .05) as compared with respective controls. In vitro acute stimulation by hCG on testicular tissue preparation obtained from MZD rats resulted in much less androgen production (sum of androstenedione, testosterone, and androstanediol) (72.4%, p < .001) as compared with controls. Testicular androgen contents (sum of androstenedione, testosterone, and androstanediol) decreased significantly in MZD and SZD rats, with the latter showing the greatest decrease. SZD rats were asospermic, whereas MZD rats exhibited marked decrease in sperm counts (by 22.9%, p < .05) as compared with respective controls. The results reflect a direct action of zinc deficiency on testicular steroidogenesis and strongly support the idea that hypogonadism of zinc deficiency results mainly from changes in testicular steroidogenesis or indirectly from Leydig cell failure.
Record 35 of 109 in MEDLINE(R)+ (1995-1997)
TI: Testis damage induced by zinc deficiency in rats.
AU: Merker,-H-J; Gunther,-T
SO: J-Trace-Elem-Med-Biol. 1997 Apr; 11(1): 19-22
AB: Male Wistar rats were fed a Zn-deficient diet (1.2 mg/kg of Zn) for 28 days. Testes were then studied by light and electron microscopy. Zn deficiency induced necroses of precursors of germ cells leading to tubular atrophy and affected differentiation of spermatids. This was expressed by the occurrence of 2-4 axoneme-dense fibre-mitochondria complexes in one spermatid. Moreover, outer dense fibres, which normally contain 90% of sperm Zn, were "uncoiled" and flattened. The multiplication of the axoneme-dense fibre-mitochondria complexes induced by Zn deficiency might have been produced by an increase of Fe in spermatids and an increased formation of oxygen free radicals.
Record 36 of 109 in MEDLINE(R)+ (1995-1997)
TI: Cytogenetic effects of cadmium on unfertilized oocytes in short-term zinc deficiency in hamsters.
AU: Watanabe,-T; Endo,-A
SO: Mutat-Res. 1997 Dec 12; 395(2-3): 113-8
AB: Chromosomal mutagenic effects of cadmium were examined during oogenesis in hamsters fed a zinc-deficient diet in the short term. Although mild zinc deficiency per se decreased the number of oocytes recovered, other reproductive and cytogenetic effects were not observed. On the other hand, cadmium induced a high incidence of oocyte degeneration and diploidy, which did not differ between the zinc-deficient and control groups. The mutagenic activities of cadmium were not accentuated in metaphase II oocytes of zinc-deficient hamsters. However, it appears that zinc deficiency alters the effects of cadmium on the reproductive system in female hamsters.
Record 37 of 109 in MEDLINE(R)+ (1995-1997)
TI: Di(2-ethylhexyl) phthalate induces a functional zinc deficiency during pregnancy and teratogenesis that is independent of peroxisome proliferator-activated receptor-alpha.
AU: Peters,-J-M; Taubeneck,-M-W; Keen,-C-L; Gonzalez,-F-J
SO: Teratology. 1997 Nov; 56(5): 311-6
AB: Di(2-ethylhexyl) phthalate (DEHP) is a peroxisome proliferator whose administration to rodents induces a pleiotropic response mediated by the peroxisome proliferator-activated receptor-alpha (PPAR alpha). The mechanisms underlying DEHP-induced reproductive toxicity and teratogenicity are not well understood but could be the result of an alteration in gene expression by PPAR alpha. Additionally, phthalate exposure is known to impair fetal zinc (Zn) levels during pregnancy. In this work, we investigated whether the reproductive toxicity and teratogenicity of DEHP are mediated by PPAR alpha and whether the receptor influences maternal and/or embryonic Zn metabolism. Pregnant female mice, homozygous wild-type (+/+) or PPAR alpha -null (-/-), were intubated with either vehicle alone or 1,000 mg DEHP/kg body weight on gestation day (GD) 8 and 9. Pregnancy outcome was evaluated on GD10 and GD18 in two cohorts of animals. Compared to controls, DEHP administration resulted in maternal toxicity, embryo/ fetal toxicity, and teratogenicity in both (+/+) and (-/-) mice. Maternal liver mRNA for cytochrome P-450 4A1 (CYP4A1) was higher in DEHP-treated (+/+) mice but not in DEHP-treated (-/-) mice on GD10, consistent with their respective phenotype. Maternal liver MT and Zn levels were significantly higher than in controls on GD10. In addition, embryonic Zn content was significantly lower in both genotypes treated with DEHP compared to controls. Results from this work show that DEHP-induced reproductive toxicity, teratogenicity, and altered Zn metabolism are not mediated through PPAR alpha-dependent mechanisms. In addition, this work suggests that DEHP-induced alterations in Zn metabolism contribute to the mechanisms underlying DEHP-induced reproductive toxicity and teratogenicity.
CN: HD01743HDNICHD; HD26777HDNICHD
Record 38 of 109 in MEDLINE(R)+ (1995-1997)
TI: In vivo and in vitro developmental toxicity in LPS-induced zinc-deficient rabbits.
AU: Pitt,-J-A; Zoellner,-M-J; Carney,-E-W
SO: Reprod-Toxicol. 1997 Nov-Dec; 11(6): 771-9
AB: Lipopolysaccharide (LPS) was used to induce maternal hypozincemia in order to test the hypothesis that altered zinc homeostasis is developmentally toxic in the rabbit. Treatment of dams on Gestation Day (GD) 8 with LPS (0.67 microgram/kg i.v.) caused total resorption of 78% (7 of 9) of the litters whereas GD 10 treatment increased the percentage of resorbed implantations (18-fold), but resulted in only 14% (1 of 7) totally resorbed litters. Cotreatment with zinc oxide (ZnO) on GD 10 decreased the resorption rate by 44%, indicating that hypozincemia was partially responsible for the resorptions. However, ZnO had no effect on resorption rate in GD 8 LPS-treated dams. No malformations were observed with LPS dosing on either gestation day. To determine whether LPS-induced Zn deficiency had any direct effects on rabbit embryos, normal GD 9 embryos were cultured for 48 h in serum from LPS-treated dams (0.53 +/- 0.01 microgram/mL Zn) or from controls (1.74 +/- 0.07 micrograms/mL Zn). Embryo growth and development were normal in both groups, indicating a lack of any direct embryo effects of Zn deficiency. Finally, maternal plasma progesterone and the Zn content of conceptus tissues were measured 24 h after LPS injection on GD 10. Despite a marked decrease in maternal serum Zn, no significant changes in embryo, visceral yolk sac, yolk sac cavity-exoceolomic fluid, or placental Zn were found. However, maternal progesterone levels were decreased 33 and 28% in the LPS and LPS + ZnO groups, respectively. Taken together, these results indicate that rabbits may differ from rodent species in their lesser susceptibility to the teratogenic potential of transient maternal Zn deficiency, as well as in their resistance to conceptus Zn changes. Nonetheless, Zn deficiency may be responsible for an increase in resorption rate in the rabbit.
Record 39 of 109 in MEDLINE(R)+ (1995-1997)
TI: Developmental toxicity of dietary zinc deficiency in New Zealand white rabbits.
AU: Pitt,-J-A; Zoellner,-M-J; Carney,-E-W
SO: Reprod-Toxicol. 1997 Nov-Dec; 11(6): 781-9
AB: Chemically induced maternal Zn deficiency has been shown previously to cause terata and increase embryonic loss in rodents. To examine the potential effects of Zn deficiency in the rabbit, a major developmental toxicity test species, rabbit dams were fed an ethylenediamine-tetraacetic acid-washed alfalfa-based Zn-deficient diet (-Zn) or the same diet replete with 80 ppm Zn (control) from Gestation Day (GD) 0 through 20. A third group of animals was pair fed to match the mean daily feed consumption levels of the < 2 ppm Zn group. By GD 7, maternal serum Zn levels of the -Zn dams were decreased 56% and reached a nadir with a 75% decrease of serum Zn by GD 14. Zinc concentrations in the visceral yolk sac and visceral yolk sac-exoceolomic fluid were decreased 30% and 50%, respectively, by GD 11. Although GD 11 embryonic Zn levels were not affected, the embryos from Zn-deficient dams exhibited decreased head length, somite number, and total protein. On GD 28, a significant increase in resorptions/litter was noted in the -Zn group, and the incidence of totally resorbed litters of the -Zn group was greater than laboratory historical control values. No terata were observed in GD 28 fetuses. This study indicates that Zn deficiency occurring during the standard dosing period of guideline rabbit developmental toxicity studies may be associated with a modest increase in resorption rate and a transient inhibition of embryonic growth, but in contrast to rodent species, does not appear to be teratogenic.
Record 40 of 109 in MEDLINE(R)+ (1995-1997)
TI: Dietary zinc deficiency alters 5 alpha-reduction and aromatization of testosterone and androgen and estrogen receptors in rat liver.
AU: Om,-A-S; Chung,-K-W
SO: J-Nutr. 1996 Apr; 126(4): 842-8
AB: We studied the effects of zinc deficiency on hepatic androgen metabolism and aromatization, androgen and estrogen receptor binding, and circulating levels of reproductive hormones in freely fed, pair-fed and zinc deficient rats. Hepatic conversion of testosterone to dihydrotestosterone was significantly less, but formation of estradiol from testosterone was significantly greater in rats fed the zinc-deficient diet compared with freely fed and pair-fed control rats. There were significantly lower serum concentrations of luteinizing hormone, estradiol and testosterone in rats fed the zinc-deficient diet. No difference in the concentration of serum follicle-stimulating hormone was observed between the zinc-deficient group and either control group. Scatchard analyses of the receptor binding data showed a significantly higher level of estrogen receptor in zinc-deficient rats (36.6 +/- 3.4 fmol/mg protein) than in pair-fed controls (23.3 +/- 2.2 fmol/mg protein) and a significantly lower level of androgen binding sites in rats fed the zinc-deficient diet (6.7 +/- 0.7 fmol/mg protein) than in pair-fed control rats (11.3 +/- 1.2 fmol/mg protein). There were no differences in hepatic androgen and estrogen receptor levels between freely fed and pair-fed controls. These findings indicate that zinc deficiency reduces circulating luteinizing hormone and testosterone concentrations, alters hepatic steroid metabolism, and modifies sex steroid hormone receptor levels, thereby contributing to the pathogenesis of male reproductive dysfunction.
Record 41 of 109 in MEDLINE(R)+ (1995-1997)
TI: Changes in distribution of labile zinc in mouse spermatozoa during maturation in the epididymis assessed by the fluorophore Zinquin.
AU: Zalewski,-P-D; Jian,-X; Soon,-L-L; Breed,-W-G; Seamark,-R-F; Lincoln,-S-F; Ward,-A-D; Sun,-F-Z
SO: Reprod-Fertil-Dev. 1996; 8(7): 1097-105
AB: The Zn(II)-specific fluorophore Zinquin was used to determine the regional distribution of free or loosely-bound Zn(II) in mouse spermatozoa. Spermatozoa from the testes exhibited bright fluorescence over the entire head; those from the caput epididymides generally fluoresced more brightly in the post-acrosomal region; and spermatozoa from the caudae epididymides fluoresced less brightly, with foci of fluorescence over the sperm head which were lost after extraction with Triton X-100 and hence appeared to be membrane-associated. Treatment of cauda sperm with sodium dodecyl sulfate resulted in a bright uniform Zinquin fluorescence in the heads, similar to that observed in caput sperm, indicating that the two types of sperm have similar amounts of head Zn(II) but that the availability of Zn(II) for binding Zinquin is different. By contrast, the intensity of tail fluorescence was similar in spermatozoa from different regions of the male reproductive tract and was largely unaffected by Triton X-100 extraction, consistent with an intracellular location. Similar differences were observed between caput sperm and cauda sperm in the rat. It is concluded that visualization and measurement of free or loosely-bound Zn(II) in subcellular compartments of spermatozoa should facilitate investigation of the role of this metal in the development and function of spermatozoa and abnormalities that might accompany infertility and Zn(II) deficiency.
Record 42 of 109 in MEDLINE(R)+ (1995-1997)
TI: Light and electron microscopic changes in the ovary of zinc deficient BALB/c mice.
AU: Kaswan,-S; Bedwal,-R-S
SO: Indian-J-Exp-Biol. 1995 Jul; 33(7): 469-79
AB: Female BALB/c strain of mice fed on Zn deficient diet for 2-, 4- and 6- weeks exhibited prolonged diestrous phase with only VII types of follicles instead of VIII as compared to their respective control and pairfed. Light microscopic studies displayed increased atresia, cessation of oogenesis and ovulation, degeneration of follicular cells of zona granulosa, clumped chromatin of oocyte and disrupted zona pellucida and corona radiata. Ultrastructural studies of peripheral follicular and theca interstitial cells of type VI and VII follicles revealed swollen mitochondria, dilated ERs (free of RNP particles), increased lysosomes, several necrotic areas of cytoplasm and pyknotic nuclei. Conclusively, Zn deficiency may lead to (1) reduction in energy, protein intake and in secretion of GnRH by hypothalamus and LH and FSH by hypophysis, (2) increased synthesis and/or secretion of prolactin. (3) reduced output of estrogen, and (4) eventually slow growth or arrest of ovulation or atresia of the growing follicles in the ovary.
Record 43 of 109 in MEDLINE(R)+ (1995-1997)
TI: Effect of zinc deficiency induced before and during pregnancy on the survival of female rats and their pups.
AU: Braga-Costa,-T-M; De-Oliveira,-L-M; Vannucchi,-H
SO: Braz-J-Med-Biol-Res. 1995 May; 28(5): 569-74
AB: The objective of the present study was to determine the consequences of Zn2+ deficiency on the gestational process. The study was conducted on adult Wistar virgin female rats fed isocaloric diets containing 16% protein and different Zn2+ concentrations, i.e., 2 ppm (severe restriction), 6 ppm (moderate restriction), and 20 ppm (control). Rats received the diets and water ad libitum for 7, 14 or 21 days before mating and throughout pregnancy. Survival of dams and pups decreased with increasing Zn2+ restriction and with time of exposure to the deficient diet. Mean survival rate for control dams and pups was 100%, whereas severe restriction (2 ppm for 21 days premating and during pregnancy) resulted in survival rates of 25% and 0 for dams and pups, respectively. Dam and pup survival rates for moderate restriction (6 ppm) for the same period were 83% and 72%, respectively. These results indicate the importance of Zn2+ before and during pregnancy and show that Zn2+ deficiency causes metabolic alterations which impair normal reproductive processes.
Record 44 of 109 in MEDLINE(R)+ (1993-1994)
TI: Altered Zn status by alpha-hederin in the pregnant rat and its relationship to adverse developmental outcome.
AU: Daston,-G-P; Overmann,-G-J; Baines,-D; Taubeneck,-M-W; Lehman-McKeeman,-L-D; Rogers,-J-M; Keen,-C-L
SO: Reprod-Toxicol. 1994 Jan-Feb; 8(1): 15-24
AB: The hypothesis that an acute-phase reaction in the pregnant animal causes a systemic redistribution of Zn, resulting in a transient but developmentally adverse Zn deficiency in the embryo, was tested by treating pregnant rats during organogenesis with alpha-hederin, an agent reported to induce substantial metallothionein (MT) synthesis in rat liver, and determining hepatic MT concentration, hepatic and plasma Zn concentration, and systemic distribution of a pulse of 65Zn after treatment. Developmental toxicity was assessed by evaluating morphologic development in term fetuses. A single dose of alpha-hederin, injected sc at dosages of 3 to 300 mumol/kg, caused an acute phase response, indicated by decreased Fe and Zn, and increased Cu, alpha 1-acid glycoprotein, and ceruloplasmin concentration in plasma, along with a dosage-related increase in maternal hepatic MT concentration. The maximum induction of MT was 11 to 15-fold greater than control and occurred at dosages of 30 mumol/kg and higher, and MT concentration reached its peak 12 to 24 h after treatment. Zn concentration in liver and liver cytosol increased along with MT, reaching a maximum level at dosages of 30 mumol/kg and higher. Plasma Zn concentration decreased after alpha-hederin treatment to a level approximately 75% of control at a dosage of 30 mumol/kg and 50% of control at 300 mumol/kg. Therefore, hepatic MT induction was associated with most, but not all, of the decrease in plasma Zn concentration. Zn distribution was evaluated by giving an oral pulse of 65Zn 8 h after treatment with 0, 30, or 300 mumol/kg alpha-hederin on gestation day 11, and measuring 65Zn levels 18 h after treatment. The fraction of 65Zn distributed to the liver of treated rats (either dosage) was twice that of control, but distribution of 65Zn to other maternal tissues was decreased. 65Zn accumulation by conceptuses was significantly decreased, attributable to decreased accumulation in decidua, but not in visceral yolk sacs or embryos; however, at this stage of development the decidua accounts for a greater quantity of Zn than either of the other products of conception and may serve as the Zn-storing tissue for the conceptus. Both 30 and 300 mumol/kg increased resorption incidence, and 300 mumol/kg also decreased fetal weight and increased the incidence of abnormal fetuses. Serum collected from rats two hours after alpha-hederin treatment (i.e., before the onset of MT synthesis) supported rat embryo development in vitro, whereas serum collected 18 h after treatment did not. Adding Zn to this serum restored normal embryonic development.(ABSTRACT TRUNCATED AT 400 WORDS)
Record 45 of 109 in MEDLINE(R)+ (1993-1994)
TI: Altered maternal zinc metabolism following exposure to diverse developmental toxicants.
AU: Taubeneck,-M-W; Daston,-G-P; Rogers,-J-M; Keen,-C-L
SO: Reprod-Toxicol. 1994 Jan-Feb; 8(1): 25-40
AB: It has been hypothesized that one mechanism contributing to the developmental toxicity of some xenobiotics is an embryonic/fetal zinc (Zn) deficiency that occurs secondary to toxicant-induced changes in maternal Zn metabolism. We studied the influence of diverse toxicants (urethane, ethanol, melphalan, arsenic, and alpha-hederin) on maternal-embryonic Zn metabolism and maternal liver metallothionein (MT) induction in Sprague-Dawley rats given a 65Zn-labelled meal by gavage 8 h after toxicant exposure and killed 10 h later on gestation day 12.5. Exposure to the toxicants resulted in increases in maternal hepatic MT concentrations that generally exceeded that which could be accounted for by reductions in food intake. 65Zinc retention was higher in maternal liver and lower in the products of conception in the toxicant-exposed groups. Strong linear relationships were found; as maternal liver MT concentrations increased, 65Zn retention in maternal liver was increased and 65Zn distribution to the conceptuses was decreased. These results support the hypothesis that diverse insults can produce developmental toxicity, in part, by altering maternal and embryonic Zn metabolism.
Record 46 of 109 in MEDLINE(R)+ (1993-1994)
TI: Zinc, copper and selenium in reproduction.
AU: Bedwal,-R-S; Bahuguna,-A
SO: Experientia. 1994 Jul 15; 50(7): 626-40
AB: Of the nine biological trace elements, zinc, copper and selenium are important in reproduction in males and females. Zinc content is high in the adult testis, and the prostate has a higher concentration of zinc than any other organ of the body. Zinc deficiency first impairs angiotensin converting enzyme (ACE) activity, and this in turn leads to depletion of testosterone and inhibition of spermatogenesis. Defects in spermatozoa are frequently observed in the zinc-deficient rat. Zinc is thought to help to extend the functional life span of the ejaculated spermatozoa. Zinc deficiency in the female can lead to such problems as impaired synthesis/secretion of (FSH) and (LH), abnormal ovarian development, disruption of the estrous cycle, frequent abortion, a prolonged gestation period, teratogenicity, stillbirths, difficulty in parturition, pre-eclampsia, toxemia and low birth weights of infants. The level of testosterone in the male has been suggested to play a role in the severity of copper deficiency. Copper-deficient female rats are protected against mortality due to copper deficiency, and the protection has been suggested to be provided by estrogens, since estrogens alter the subcellular distribution of copper in the liver and increase plasma copper levels by inducing ceruloplasmin synthesis. The selenium content of male gonads increases during pubertal maturation. Selenium is localized in the mitochondrial capsule protein (MCP) of the midpiece. Maximal incorporation in MCP occurs at steps 7 and 12 of spermatogenesis and uptake decreases by step 15. Selenium deficiency in females results in infertility, abortions and retention of the placenta. The newborns from a selenium-deficient mother suffer from muscular weakness, but the concentration of selenium during pregnancy does not have any effect on the weight of the baby or length of pregnancy. The selenium requirements of a pregnant and lactating mother are increased as a result of selenium transport to the fetus via the placenta and to the infant via breast milk.
Record 47 of 109 in MEDLINE(R)+ (1993-1994)
TI: Effects of dietary zinc deficiency on the reproductive system of young male sheep: testicular growth and the secretion of inhibin and testosterone.
AU: Martin,-G-B; White,-C-L; Markey,-C-M; Blackberry,-M-A
SO: J-Reprod-Fertil. 1994 May; 101(1): 87-96
AB: The effects of dietary zinc deficiency on testicular development in young Merino rams (initial live mass, 22 kg) were tested. Four groups of five rams were fed ad libitum with diets containing 4, 10, 17 or 27 micrograms Zn g-1. To control the effects of loss of appetite caused by zinc deficiency, a fifth group (pair-fed control) was fed the diet containing 27 micrograms Zn g-1, but the amount of feed offered was restricted to that eaten voluntarily by the zinc deficient (4 micrograms Zn g-1) rams they were paired with. After 96 days on the diets, epididymal and testicular masses did not differ significantly between the animals fed 10, 17 or 27 micrograms Zn g-1 ad libitum, but were significantly lower in pair-fed controls, and lowest in the zinc-deficient animals. Testicular responsiveness to LH, as measured by testosterone production, increased substantially in most rams as the experiment progressed, the only exception being the zinc-deficient group, in which the response to LH was lower than in any of the other groups. Testicular concentrations of zinc and testosterone were lower in the zinc-deficient animals than in all the other groups. Plasma inhibin concentrations fell as the experiment progressed in rams fed 17 and 27 micrograms Zn g-1 ad libitum, but not in the other groups. The pair-fed control rams had smaller seminiferous tubules and less lumen development than did the controls fed ad libitum (27 micrograms Zn g-1), which were similar to the animals fed 10 or 17 micrograms Zn g-1. In zinc-deficient rams, the tubule development was further retarded and the interstitial regions were more extensive than in the other groups. We conclude that the overall effect of zinc deficiency on testicular development is due to a combination of a non-specific effect (low gonadotrophin concentrations caused by the low feed intake) and a specific effect due to the lack of zinc. The zinc-specific effect is localized within the testis where it reduces the development of the capacity to produce testosterone, leading to low intratesticular concentrations of testosterone, a critical factor for the growth, development and function of the seminiferous tubules.
Record 48 of 109 in MEDLINE(R)+ (1993-1994)
TI: Histological and biochemical changes in testis of zinc deficient BALB/c strain of mice.
AU: Bedwal,-R-S; Edwards,-M-S; Katoch,-M; Bahuguna,-A; Dewan,-R
SO: Indian-J-Exp-Biol. 1994 Apr; 32(4): 243-7
AB: Zinc, protein, cholesterol, phospholipids, alkaline phosphatase (AlPase), acid phosphatase (AcPase), adenosine-5-triphosphatase(ATPase) and histology were studied in testis of zinc-deficient mice. Zinc and protein decreased in the 3-week experiment whereas they increased in the 6-week experiment. Zinc is involved in several functions of the cell and is regulated by hormones. Inhibition of spermatogenesis indicates for decreased zinc levels in 3-week whereas the increase in 6-week experiment indicates for accumulation of zinc in oedomatous fluid and uncontrolled diffusion of zinc across the blood testis barrier. Glycogen decreased in the 3-week as well as 6-week experiments due to blockage of androgen and spermatogenesis. Cholesterol and phospholipids increased in the 3-week experiment and decreased in 6-week experiment as both the parameters are related to steroidogenesis. Zinc deficiency leads to aspermatogenic condition and comparatively less injury to non-germinal cells. This could have blocked the transport of material across the testis barrier and therefore might have increased AlPase levels. Increased AcPase, probably represents lysosomal enzymes, as the cell debris of disorganised epithelium are to be digested and removed. ATPase increased in 3-week experiment and can be correlated to increased demands of energy of testicular cells to overcome the insults of zinc deficiency whereas the decrease in 6-week experiment could be as a result of inhibition of spermatogenesis.
Record 49 of 109 in MEDLINE(R)+ (1993-1994)
TI: Zinc: health effects and research priorities for the 1990s.
AU: Walsh,-C-T; Sandstead,-H-H; Prasad,-A-S; Newberne,-P-M; Fraker,-P-J
SO: Environ-Health-Perspect. 1994 Jun; 102 Suppl 25-46
AB: This review critically summarizes the literature on the spectrum of health effects of zinc status, ranging from symptoms of zinc deficiency to excess exposure. Studies on zinc intake are reviewed in relation to optimum requirements as a function of age and sex. Current knowledge on the biochemical properties of zinc which are critical to the essential role of this metal in biological systems is summarized. Dietary and physiological factors influencing the bioavailability and utilization of zinc are considered with special attention to interactions with iron and copper status. The effects of zinc deficiency and toxicity are reviewed with respect to specific organs, immunological and reproductive function, and genotoxicity and carcinogenicity. Finally, key questions are identified where research is needed, such as the risks to human health of altered environmental distribution of zinc, assessment of zinc status in humans, effects of zinc status in relation to other essential metals on immune function, reproduction, neurological function, and the cardiovascular system, and mechanistic studies to further elucidate the biological effects of zinc at the molecular level.
CN: FDAU000457FDFDA; NIDDKDK31401DKNIDDK
Record 50 of 109 in MEDLINE(R)+ (1993-1994)
TI: Zinc deficiency affects the activity and protein concentration of angiotensin-converting enzyme in rat testes.
AU: Reeves,-P-G; Rossow,-K-L
SO: Proc-Soc-Exp-Biol-Med. 1993 Jul; 203(3): 336-42
AB: Zinc (Zn) deficiency causes hypogonadism in a number of different species. Previous work has shown that Zn deficiency reduces the activity of angiotensin-converting enzyme (ACE), a Zn-dependent enzyme, in the testes of prepubertal rats. These studies were designed to determine whether this effect was caused by a change in the concentration of ACE protein. Thirty-five male rats at 26 days of age were divided into three groups. One group was fed ad libitum a Zn-adequate diet (40 mg/kg); another group was fed a similar diet, but deficient in Zn (< 1.0 mg/kg); a third group was pair-fed to the deficient group. After 4 weeks on these regimens, all rats in the ad libitum-fed group and half of the rats in each of the deficient and pair-fed groups were sacrificed, and tissues were collected for analysis. The remaining animals in the Zn-deficient and pair-fed groups were fed a Zn-adequate diet ad libitum for another 2 weeks, then sacrificed. With the use of an enzyme-linked immunosorbent assay for testicular ACE protein, the effect of these treatments on the concentration of ACE protein in testes was determined. After 4 weeks, ACE activity in testes of the Zn-deficient rats was reduced by 74% compared to that in the ad libitum-fed controls. This was accompanied by a 64% reduction in the amount of ACE protein in the testes. There was not a significant effect of pair-feeding. Refeeding Zn-deficient rats a Zn-adequate diet for 2 weeks restored ACE protein concentrations and ACE activity to values not significantly different from those in pair-fed controls. Soluble ACE, but not particulate ACE, of the epididymis was significantly reduced by Zn deficiency. Because the ACE activity of testes has been found primarily in the germinal cells, and soluble ACE in the epididymis is derived from the testes, these findings suggest that the effects of Zn deficiency on testicular and epididymal ACE is caused by an impairment of spermatid development.
Record 51 of 109 in MEDLINE(R)+ (1993-1994)
TI: Zinc, iron, and copper contents of Xenopus laevis oocytes and embryos.
AU: Nomizu,-T; Falchuk,-K-H; Vallee,-B-L
SO: Mol-Reprod-Dev. 1993 Dec; 36(4): 419-23
AB: Zinc is essential for vertebrate development; its deficiency results in multiple congenital malformations. Knowledge of the zinc biochemistry that underlies embryologic development is very limited. This has led us to investigate the zinc, iron, and copper contents of Xenopus laevis oocytes and embryos. Stage 1-6 oocytes, isolated from ovaries, and stage 1-40 embryos, obtained by in vitro fertilization techniques, were washed in metal-free water prior to digestion by 70% ultrapure HNO3. The metal content of the digests was analyzed by atomic absorption spectrometry. Stage 6 oocytes contain 65.8 +/- 4, 31.1 +/- 3, and 0.68 +/- 0.2 ng of zinc, iron and copper, respectively. The corresponding concentrations are 1, 0.5, and 0.01 mM in 1 microliter eggs. The metal content varies as a function of egg maturation. The zinc content increases from 3-7 to > 60 ng by stages 3 and 6, respectively. A similar pattern is noted for iron, which increases from 2-5 to 30 ng at analogous stages. In contrast, the copper content remains virtually unchanged in oocytes undergoing maturation. Importantly, the total of all three metals does not vary throughout the first 50 stages of development, when all tadpole organs are forming. Hence, the full complement of zinc, iron, and copper needed for incorporation into apoproteins during development is already present at a time when oocyte maturation is completed. The specific metalloproteins that store, donate, and accept these metals during induction and organogenesis and the alterations caused by metal deficiency can now be identified.
Record 52 of 109 in MEDLINE(R)+ (1993-1994)
TI: The biochemical basis of zinc physiology.
AU: Vallee,-B-L; Falchuk,-K-H
SO: Physiol-Rev. 1993 Jan; 73(1): 79-118
Record 53 of 109 in MEDLINE(R)+ (1993-1994)
TI: Low zinc intake during pregnancy: its association with preterm and very preterm delivery.
AU: Scholl,-T-O; Hediger,-M-L; Schall,-J-I; Fischer,-R-L; Khoo,-C-S
SO: Am-J-Epidemiol. 1993 May 15; 137(10): 1115-24
AB: Zinc affects growth, development, and reproduction. However, the effect of poor maternal zinc nutriture, usually measured as plasma zinc, on poor pregnancy outcome has not been consistent. The influence of dietary zinc on pregnancy outcome was examined in a cohort of 818 pregnant girls and women from a poor urban community in Camden, New Jersey (1985-1990). Zinc intake in this sample was 11.1 mg/day, a level ascertained from averaged 24-hour dietary recalls during pregnancy. Gravidas with low zinc intake (< or = 6 mg/day, amounting to 40% of the recommended dietary allowance for pregnancy) had lower caloric intake and multivitamin usage as well as a higher incidence of inadequate weight gain during pregnancy and iron deficiency anemia at entry to prenatal care compared with those with higher intakes. A low zinc intake was associated with approximately a twofold increase in the risk of low birth weight (< 2,500 g) after controlling for calories and other confounding variables. The risk of preterm delivery (< 37 completed weeks) was also increased, particularly when rupture of the membranes preceded the onset of labor (adjusted odds ratio = 3.46, 95% confidence interval 1.04-11.47). A low intake of dietary zinc earlier in pregnancy was associated with a greater than threefold increase in the risk of very preterm delivery (< 33 completed weeks). In conjunction with iron deficiency anemia at entry to prenatal care, the adjusted odds ratio for very preterm delivery with low zinc intake was 5.44 (95% confidence interval 1.58-18.79). Among the urban poor, a marginal zinc intake during pregnancy may play an important role in the duration of gestation and is associated with increased risk of preterm and very preterm delivery.
Record 54 of 109 in MEDLINE(R)+ (1993-1994)
TI: Zinc-silicon interactions influencing sperm chromatin integrity and testicular cell development in the rat as measured by flow cytometry.
AU: Evenson,-D-P; Emerick,-R-J; Jost,-L-K; Kayongo-Male,-H; Stewart,-S-R
SO: J-Anim-Sci. 1993 Apr; 71(4): 955-62
AB: Flow-cytometric procedures were used to determine effects of dietary Zn and Si variations on rat testicular cell development, including integrity of caudal epididymal sperm chromatin structure defined as the susceptibility of DNA to denaturation in situ. Concentrations of 4 (deficient), 12 (adequate), and 500 (excessive) mg of Zn/kg of diet were used with Si concentrations of 0 (low), 540 (medium), and 2,700 (high) mg/kg of diet in a 3 x 3 factorial arrangement. Three-week-old Sprague-Dawley male rats were fed the experimental diets for 8 wk. Rats fed the Zn-deficient/Si-low diet demonstrated significant deviations in the ratio of testicular cell types present, including a reduction of S phase and total haploid cells. Furthermore, approximately 50% of epididymal sperm had a significant decrease in resistance to DNA denaturation in situ. In the Zn-deficient/Si-medium treatment, the effects of Si on animal and testicular growth, distribution of testicular cell types, and sperm chromatin structure integrity were quite similar to the effects of the Zn-adequate diets. A toxic effect of Zn on sperm chromatin structure integrity observed in the Zn-excess/Si-medium treatment seemed to be counteracted by Si in the Zn-excess/Si-high treatment. Silicon at medium and high levels seems to affect Zn metabolism through potentiation and antagonistic reactions, respectively. Zinc deficiency likely disrupts the normal sperm chromatin quaternary structure in which Zn plays a role by providing stability and resistance to DNA denaturation in situ.
Record 55 of 109 in MEDLINE(R)+ (1993-1994)
TI: Influence of periconceptional zinc deficiency on embryonic plasma membrane function in mice.
AU: Peters,-J-M; Wiley,-L-M; Zidenberg-Cherr,-S; Keen,-C-L
SO: Teratog-Carcinog-Mutagen. 1993; 13(1): 15-21
AB: Periconceptional Zn deprivation can affect development of 2- and 4-cell mouse embryos in vitro as evidenced by fewer cells per embryo and delayed blastocyst development after 72 h in culture. One mechanism by which this could be occurring is through changes in oocyte and embryonic membrane structure/function. To test this idea, 3H-glycine uptake was measured in unfertilized oocytes and preimplantation embryos recovered from mice fed control (+Zn; 50 micrograms Zn/g diet) or low Zn (-Zn; < or = 0.4 micrograms Zn/g diet) diets for 6 days. In a second experiment, we assessed the in vitro development of preimplantation embryos in medium designed to inhibit cavitation through changes in membrane-associated sodium flux. Preimplantation embryos from -Zn and +Zn mice recovered on day 1 of gestation were cultured in medium containing 147.2 mM sodium (normal) or 123 mM sodium (low sodium) for 48 h. In experiment 1, glycine uptake was similar in embryos from +Zn and -Zn mice, suggesting that the impaired in vitro development of embryos from -Zn mice is not due to gross changes in sodium-dependent cell membrane function. In experiment 2, embryos recovered from -Zn mice and cultured in normal sodium medium contained fewer cells than controls. Embryos from both groups cultured in low sodium medium contained fewer cells than their normal sodium controls; the percent difference in cell number was 50 +/- 8% and 56 +/- 11% for embryos from +Zn and -Zn mice, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
CN: HD07131HDNICHD; HD16330HDNICHD; HD01743HDNICHD
Record 56 of 109 in MEDLINE(R)+ (1993-1994)
TI: Testosterone increases TRH biosynthesis in epididymis but not heart of zinc-deficient rats.
AU: Pekary,-A-E; Lukaski,-H-C; Mena,-I; Smith,-S-M; Bhasin,-S; Hershman,-J-M
SO: Peptides. 1993 Mar-Apr; 14(2): 315-24
AB: Enzymes responsible for the posttranslational processing of precursor proteins to form alpha-amidated peptide hormones require the availability of several cofactors, including zinc, copper, and ascorbic acid. For this reason, we studied the effects of 6 weeks of a zinc-deficient diet (ZD1; 1 microgram zinc per g diet), pair-feeding (PF), and marginal zinc deficiency (ZD6; 6 micrograms zinc per g diet) compared to a control diet (36 micrograms/g zinc) on the conversion of prepro-TRH to TRH in epididymides, testes, prostate, pancreas, and heart of young adult, male Sprague-Dawley rats. In the epididymis, severe zinc deficiency (ZD1 diet) reduced TRH and TRH-like peptides to undetectable levels. In ZD6 animals, TRH was selectively inhibited 80%, while pair-feeding increased all of these peptide levels compared to controls. A similar effect of zinc deficiency on the TRH precursor peptides was observed. A quantitative loss of TRH from the testes of ZD1 was also observed. Zinc deficiency results in a substantial reduction in body weight and testosterone production in male rats. Exogenous testosterone (T) supplementation of ZD1 rats resulted in a selective increase in the TRH concentration of the epididymis but not of the heart. The change in steady-state levels of TRH precursor peptides in the hearts of the ZD1+T rats was consistent with a reduction in the activity of the zinc-dependent carboxypeptidase H enzyme. We conclude that severe zinc deficiency inhibits TRH biosynthesis in reproductive tissues of the male rat due to the combined effects of hypogonadism and inhibition of the zinc-dependent carboxypeptidase H.
Record 57 of 109 in MEDLINE(R)+ (1990-1992)
TI: The role of zinc in reproduction. Hormonal mechanisms.
SO: Biol-Trace-Elem-Res. 1992 Jan-Mar; 32363-82
AB: Zinc is a very important element in the reproductive cycle of species. In humans, it is necessary for the formation and maturation of spermatozoa, for ovulation, and for fertilization. During pregnancy, zinc deficiency causes a number of anomalies: spontaneous abortion, pregnancy-related toxemia, extended pregnancy or prematurity, malformations, and retarded growth. Delivery is adversely affected by deficiency. These different effects of zinc can be explained by its multiple action on the metabolism of androgen hormones, estrogen and progesterone, together with the prostaglandins. Nuclear receptors for steroids are all zinc finger proteins. Zinc supplementation has already proven beneficial in male sterility and in reducing complications during pregnancy. However, it would be worth conducting larger-scale trials to confirm these beneficial effects.
Record 58 of 109 in MEDLINE(R)+ (1990-1992)
TI: Effects of dietary zinc deficiency on gonadotrophin secretion and testicular growth in young male sheep.
AU: Martin,-G-B; White,-C-L
SO: J-Reprod-Fertil. 1992 Nov; 96(2): 497-507
AB: The hypothesis that the secretion of gonadotrophins would be reduced by zinc deficiency was tested in five groups of four young Merino rams (initial liveweight 22 kg). Four groups were fed ad libitum with diets containing 4, 10, 17 or 27 micrograms Zn g-1. The effects of loss of appetite on the deficient diet was controlled by feeding a fifth group (pair-fed control) at a rate of 27 micrograms Zn g-1, but the amount of feed offered was restricted to that eaten voluntarily by the deficient (4 micrograms Zn g-1) group. Blood was sampled every 20 min for 32 h on two occasions before the treatments were imposed and 96 days later, at the end of the experiment. The rams were injected with gonadotrophin-releasing hormone (GnRH; 10 ng kg-1 i.v.) after each serial sampling, and with naloxone (1 mg kg-1 i.v.) 24 h after the end of the final GnRH test. In the group that were fed the diet with the lowest zinc content, the concentration of zinc in blood plasma was reduced to 18% of that in the pair-fed controls (P < 0.05) and was within the deficient range. The appetite of the deficient rams was half that of the controls fed 27 micrograms Zn g-1 ad libitum and there was no increase in liveweight or testicular diameter during pubertal development. Similar, but smaller, effects were observed in the pair-fed controls. There were no significant differences between pair-fed and deficient groups in the frequency of the luteinizing hormone (LH) pulses or in the concentration of follicle-stimulating hormone (FSH), but the secretion of gonadotrophins was markedly lower in both groups than in the control rams fed ad libitum. The response to GnRH was not affected by treatment, but the increase in LH pulse frequency evoked by naloxone was lower in the deficient animals than in other groups. The animals fed zinc at intermediate rates (10-17 micrograms g-1) showed similar responses to the controls fed ad libitum. It is concluded that the specific effects of zinc deficiency on testicular function were small. Most of the reduction in testicular growth in rams fed a deficient diet was not specifically related to the trace element, but was due to the fall in energy and protein intake caused by the loss of appetite. This leads to a reduction in the frequency of GnRH pulses secreted by the hypothalamus, and to low rates of gonadotrophin secretion by the pituitary gland.
Record 59 of 109 in MEDLINE(R)+ (1990-1992)
TI: Effects of dietary zinc depletion on seminal volume and zinc loss, serum testosterone concentrations, and sperm morphology in young men.
AU: Hunt,-C-D; Johnson,-P-E; Herbel,-J; Mullen,-L-K
SO: Am-J-Clin-Nutr. 1992 Jul; 56(1): 148-57
AB: Identification of the andrological variables most sensitive to zinc depletion would expedite the diagnosis of male reproductive pathology induced by zinc deficiency. Eleven volunteers living on a metabolic ward were fed a diet composed of a mixture of a semisynthetic formula and conventional foods supplemented with ZnSO4 to supply a total of 1.4, 2.5, 3.4, 4.4, or 10.4 mg Zn/d. After an equilibration period of 28 d (10.4 mg Zn/d), all treatments were presented for 35 d each, the first four in random order and the fifth last. Compared with when they were consuming 10.4 mg Zn/d, volunteers consuming 1.4 mg Zn/d exhibited decreased semen volumes (3.30 vs 2.24 mL) and serum testosterone concentrations (26.9 vs 21.9 nmol/L), and no change in seminal zinc concentrations. Compared with 10.4 mg Zn/d, treatments of 1.4, 2.5, and 3.4 mg Zn/d decreased the total semen zinc loss per ejaculate (6.29 vs 3.81, 4.68, and 5.03 mumols/ejaculate). Seminal loss accounted for 9% of total body zinc loss when 1.4 mg Zn/d was consumed. Seminal phosphorus concentrations were elevated during all four phases of zinc depletion (28.4 vs 32.9, 31.0, 34.2, and 33.6 mmol/L). The findings suggest that serum testosterone concentrations, seminal volume, and total seminal zinc loss per ejaculate are sensitive to short-term zinc depletion in young men.
Record 60 of 109 in MEDLINE(R)+ (1990-1992)
TI: An update of the zinc deficiency theory of schizophrenia. Identification of the sex determining system as the site of action of reproductive zinc deficiency.
SO: Med-Hypotheses. 1992 Aug; 38(4): 284-91
AB: The following article updates the GZD theory of schizophrenia (1) by showing that male transmission of risk, the parental age effect, racial differences in birth seasonality, the disturbed sex ratios in the offspring of schizophrenic mothers and the association between diabetes and schizophrenia are explained by changes to zinc homeostasis. A genetic component to the disorder is now seen as unnecessary, transmission of risk by either parent, and twin concordance differences can be explained by other means. The primary site of action of GZD is identified as the putative ZFY sex determining system. Evidence suggesting that other mental disorders might be caused by GZD is also discussed.
Record 61 of 109 in MEDLINE(R)+ (1990-1992)
TI: Trace element deficiencies in cattle.
SO: Vet-Clin-North-Am-Food-Anim-Pract. 1991 Mar; 7(1): 153-215
AB: Deficiency of cobalt, copper, iron, iodine, manganese, selenium, or zinc can cause a reduction in production. Reduced production occurs most commonly when a deficiency corresponds to the phases of growth, reproduction, or lactation. Because of environmental, nutrient, disease, genetic, and drug interactions, deficiencies of single or multiple elements can occur even when the levels recommended by the National Research Council for these nutrients are being fed. Additionally, random supplementation of trace elements above National Research Council recommendations is not justified because of the negative interaction among nutrients and potential toxicosis. Evaluation of trace element status can be difficult because many disease states will alter blood analytes used to evaluate nutrient adequacy. Proper dietary and animal evaluation, as well as response to supplementation, are necessary before diagnosing a trace element deficiency.
Record 62 of 109 in MEDLINE(R)+ (1990-1992)
TI: Response of testes, epididymis, and seminal vesicle of rabbits to zinc deficiency.
AU: Eltohamy,-M-M; Younis,-M
SO: Arch-Exp-Veterinarmed. 1991; 45(1): 155-60
AB: It is the purpose of this study to determine the effects of Zn deficiency on the biochemical composition of testes, epididymis, and seminal vesicle of rabbits. An attempt is made to evaluate previous physiological studies and to correlate them with biochemical changes. 30 mature male Balady rabbits were used in this study. 1 group was fed a Zn-deficient diet, and 2 control groups were pair-fed or fed ad libitum a Zn-sufficient diet, all for a period of 120 d. There was significant reduction in the levels of hyaluronidase, alkaline phosphatase, acid phosphatase, lactic dehydrogenase, sialic acid, protein, and Zn of both testes and epididymis of Zn-deficient rabbits. Reduction in the level of glyceryl-phosphoryl choline in the epididymis of Zn-deficient rabbits was the best indicator of inhibition of epididymal secretory activity. In contrast, the cholesterol and glycogen contents of the testes were elevated. The results also showed in Zn-deficient rabbits significant reduction in androgen-sensitive parameters, namely fructose and citric acid in the seminal vesicle. Zn levels were decreased in the seminal vesicle. The results indicated that Zn deficiency caused inhibition of testicular, epididymal, and seminal vesicle function and, consequently, caused reductions in the biochemical composition of these organs.
Record 63 of 109 in MEDLINE(R)+ (1990-1992)
TI: Influence of short-term maternal zinc deficiency on the in vitro development of preimplantation mouse embryos.
AU: Peters,-J-M; Wiley,-L-M; Zidenberg-Cherr,-S; Keen,-C-L
SO: Proc-Soc-Exp-Biol-Med. 1991 Oct; 198(1): 561-8
AB: In this study, we evaluated the use of mouse preimplantation embryos as a model to study zinc deficiency-induced abnormal development. In Experiment 1, the effect of culture medium Zn concentrations on blastocyst development was studied. Preimplantation embryos (2 and 4 cells) obtained from superovulated females developed normally in media containing 0.7-30 microM Zn for up to 72 hr; higher levels of medium Zn resulted in abnormal development. In Experiment 2A, females were fed diets containing 50 (+Zn) or 0.4 (-Zn) micrograms Zn/g (760 vs 6 nmol/g, respectively) from 1 day before to 1 day after mating (3 days total). Preimplantation embryos were removed from the dams and cultured for 72 hr in 0.7 microM Zn medium. Embryos from the -Zn dams were morphologically normal at time zero; however, over the 72-hr period, these embryos tended to develop at a slower rate than controls, although compaction and cavitation frequency were similar. By the end of the 72-hr culture period, embryos from -Zn dams had significantly fewer cells than did embryos from control dams. In Experiment 2B, an extended period of maternal Zn deprivation (6 days) was used to investigate the potential for further impairment of in vitro preimplantation embryo development observed in Experiment 2A. Results from this experiment were consistent with those from Experiment 2A, in addition to providing evidence that the developmental progress of embryos obtained from mice fed Zn-deficient diets for 6 days was significantly impaired. In Experiment 3, the potential for supplemental Zn in culture medium to overcome the impairment in development due to maternal Zn deficiency was investigated. Embryos from female mice subjected to the same dietary regimen described in Experiment 2A were cultured to the blastocyst stage in medium containing Zn at a concentration of either 0.7 or 7.7 microM. Medium Zn supplementation did not improve development of embryos from dams fed Zn-deficient diets. In summary, embryos from mice fed -Zn diets for a 3- or 6-day period encompassing oocyte maturation and fertilization exhibited impaired development in vitro. This impairment was not overcome by medium Zn supplementation.
CN: HD01743HDNICHD; HD16330HDNICHD
Record 64 of 109 in MEDLINE(R)+ (1990-1992)
TI: Effects of dietary zinc deficiency on protein secretory functions of the mouse testis.
AU: Ueda,-H; Kayama,-F; Mori,-N; Doi,-Y; Fujimoto,-S
SO: Arch-Histol-Cytol. 1991 Oct; 54(4): 401-10
AB: The effects of dietary zinc deficiency on testicular protein secretion, mainly that by Sertoli cells, were examined by electron microscopy and two-dimensional polyacrylamide gel electrophoresis of [35S] methionine-labeled secretory proteins from mouse testes. Zinc deficiency caused a significant decrease in the gonadosomatic index and a distinct increase in deoxyribonucleic acid concentration. Sertoli cells maintained normal fine-structural features; junctional complexes among Sertoli cells continued to divide seminiferous tubules into basal and adluminal compartments in the zinc-deficient mouse testes. Severe atrophic changes were observed in spermatogenic cells after meiotic division in the adluminal compartment, but not in spermatogonia located in the basal compartment. Zinc replacement treatment caused spermatogenesis to recover normally. Although total protein secretion was not affected by zinc deficiency, one polypeptide spot appeared due mainly to the loss of its target spermatogenic cells. The present study indicates that zinc is indispensable for spermatogenic cells after meiosis and that testicular protein secretory functions can be preserved in the absence of zinc.
Record 65 of 109 in MEDLINE(R)+ (1990-1992)
TI: Interaction of aluminum with zinc and copper and its effects on pituitary-testicular axis: a histological study.
AU: Liu,-J-Y; Stemmer,-K-L
SO: Biomed-Environ-Sci. 1990 Mar; 3(1): 1-10
AB: To elucidate the interactions between aluminum and certain essential trace metals, an experiment was performed on rats fed diets with suboptimal or optimal levels of zinc or copper. Half of each group of animals were fed the same diet but with 1000 ppm aluminum added. Changes were noted after 120 days. Severe testicular damage was seen in rats fed either the low zinc or the low copper diet. The lesions included a wide range of spermatogenic cell degeneration and tubular atrophy. When aluminum was added to the diet, the testicular destruction of Zn-deficient rats was significantly reduced. This indicated that the presence of aluminum in the diet protected the testis against the damage caused by zinc deficiency. Pituitary glands were examined. Hypertrophy of basophiles was more pronounced in rats fed the suboptimal zinc or copper diet. When aluminum was added to their diet, the changes were reversed. The mechanisms by which aluminum protects male gonadal functions against Zn deficiency are discussed. This study is the first to demonstrate the preventive effect of aluminum against testicular damage caused by zinc deficiency.
Record 66 of 109 in MEDLINE(R)+ (1990-1992)
TI: Role of zinc in regulating the testicular function. Part 3. Histopathological changes induced by dietary zinc deficiency in testes of male albino rats.
AU: Hafiez,-A-A; el-Kirdassy,-Z-H; el-Malkh,-N-M; el-Zayat,-E-M
SO: Nahrung. 1990; 34(1): 65-73
AB: Zinc deficiency affects the testicular tissues adversely. The testes of zinc-deficient rats showed variable degrees of degeneration compared to both control and zinc-supplemented ones. Initially, there was an early pronounced spermatic arrest followed by a series of degeneration of the cellular layers constituting the seminiferous tubules in the zinc-deficient rats. Degenerative changes were additionally demonstrated in the interstitial tissue cells of the zinc-deficient rats. These histopathological observations in testes of zinc-deficient rats run in parallel provide an additional support to our previous publications in which we recorded a significant reduction in both serum and testicular levels of testosterone in the same group of animals, since spermatogenesis in rodents appeared to depend primarily on testosterone level.
Record 67 of 109 in MEDLINE(R)+ (1990-1992)
TI: The influence of dietary folate supplementation on the incidence of teratogenesis in zinc-deficient rats.
AU: Quinn,-P-B; Cremin,-F-M; O'Sullivan,-V-R; Hewedi,-F-M; Bond,-R-J
SO: Br-J-Nutr. 1990 Jul; 64(1): 233-43
AB: Two studies were conducted to investigate the possibility that pteroylmonoglutamic acid supplementation would alleviate teratogenesis in zinc-deficient rats. Pregnant rats of the Wistar strain were fed on Zn-deficient (less than 0.5 mg Zn/kg) or Zn-supplemented (75 or 95 mg Zn/kg) diets from mating until day 18.5 of gestation. The basal level of pteroylmonoglutamic acid added to all diets (0.56 mg/kg) was supplemented with 30-200 mg/kg in selected diets. Dietary Zn deprivation resulted in fetal resorption, fetal growth retardation and reduced concentrations of Zn in fetuses and maternal plasma and tibia. Low maternal body-weight at conception emerged as an important determinant of risk of resorption in Zn-deficient rats. Dietary Zn deficiency resulted in reduced maternal plasma folate concentrations and these values were inversely correlated with litter size or weight in Zn-deficient rats. Pteroylmonoglutamic acid supplementation increased maternal plasma folate concentrations, but did not reduce the high incidence of teratogenesis which occurred in Zn-deficient rats. Supplementation of Zn-deficient rats with pteroylmonoglutamic acid significantly increased the incidence of clubbed foot and tended to increase the incidence of brain or meningeal abnormalities, or both, and cleft palate, but did not reduce maternal or fetal Zn status. Pteroylmonoglutamic acid supplementation also increased the weights of Zn-supplemented control fetuses.
Record 68 of 109 in MEDLINE(R)+ (1990-1992)
TI: Zinc deficiency and dipeptidyl carboxypeptidase activity. Comparative effects on epididymis and testis of rats.
SO: Biol-Trace-Elem-Res. 1990 Jan; 24(1): 1-11
AB: Dipeptidyl carboxypeptidase (DC) is highly active in the testis and epididymis of rats and increases during pubertal development. Zinc deficiency during this period depresses the activity of DC in the testis. Experiments were conducted to determine the effects of zinc deficiency on epididymal DC activity. Comparisons were made between changes seen in this organ and those observed in testis. Three dietary treatments were used; zinc-deficient, fed ad libitum; zinc-adequate, pair-fed to the deficient group; and zinc-adequate, fed ad libitum. Results confirmed that testicular DC is affected negatively by zinc deficiency. DC activity was also lower in the epididymis of zinc-deficient rats than in control rats. These effects apparently were specific relative to changes in activity of other enzymes. Alkaline phosphatase activity in the epididymis was not affected by zinc deficiency and it was depressed in the testis. Gamma-glutamyl transferase activity in the epididymis was not affected by zinc deficiency but it was elevated in the testis. The results of this study suggest that part of the effect of zinc deficiency on sexual maturity in the male rat may be caused by reduced activity of DC. This enzyme is thought to be required for maturation and development of sperm cells.
Record 69 of 109 in MEDLINE(R)+ (1987-1989)
TI: Effect of dietary zinc and copper on peripheral blood plasma cholesterol, testosterone and histomorphology of testes in rats.
AU: Mehta,-U; Mehta,-S-N; Georgie,-G-C; Mehta,-S; Dixit,-V-P; Verma,-P-C
SO: Indian-J-Exp-Biol. 1989 May; 27(5): 469-71
AB: Total plasma cholesterol (mg/dl) significantly (P less than 0.01) decreased from 70.8 to 54.01 as the dietary Cu levels increased from 2.5 to 5 ppm at 12 pm Zn concentrations in male weanling rats. A similar trend was observed in the blood peripheral testosterone concentration at 12 ppm Zn and 2.5 ppm Cu. Histological examination of testes revealed smaller seminiferous tubules with atrophy of germinal epithelium. Also a marked loss of spermatogenic cells was observed in Zn and Cu deficient rats.
Record 70 of 109 in MEDLINE(R)+ (1987-1989)
TI: Zinc deficiency and hyperprolactinaemia are not reversible causes of sexual dysfunction in uraemia.
AU: Rodger,-R-S; Sheldon,-W-L; Watson,-M-J; Dewar,-J-H; Wilkinson,-R; Ward,-M-K; Kerr,-D-N
SO: Nephrol-Dial-Transplant. 1989; 4(10): 888-92
AB: We selected a group of male dialysis patients complaining of sexual dysfunction in whom penile vascular insufficiency and drug-induced impotence had been excluded. Monitoring of nocturnal penile tumescence was used to confirm organic disturbance. Patients with normal serum prolactin concentrations (n = 18) had significantly lower serum zinc values than normal controls (P less than 0.001) and were entered in a 6-month double-blind study comparing oral zinc acetate with placebo. Patients with elevated prolactin concentrations (n = 8) were entered in a 3-month double-blind crossover study comparing oral pergolide mesylate with placebo. In the zinc study, serum zinc concentrations increased (P less than 0.05) in the zinc-treated but not the placebo-treated group. One of nine patients receiving zinc reported improved sexual function, as did two of nine patients receiving placebo. There were no significant changes in sperm counts, nocturnal penile tumescence, testosterone, sex hormone binding globulin or gonadotrophin concentrations in either treatment group. In the pergolide study, serum prolactin values decreased (P less than 0.01) in the pergolide but not in the placebo treatment period. One patient reported improved sexual function during the pergolide treatment period and two during the placebo period. There were no significant changes in sperm counts, nocturnal penile tumescence, testosterone, sex hormone binding globulin or gonadotrophin concentrations after pergolide. These studies show no benefit of zinc or pergolide compared with placebo in the treatment of uraemic impotence.
Record 71 of 109 in MEDLINE(R)+ (1987-1989)
TI: Plasma and erythrocyte zinc concentrations in pre-eclampsia.
AU: Lao,-T-T; Chin,-R-K; Swaminathan,-R; Mak,-Y-T
SO: Eur-J-Obstet-Gynecol-Reprod-Biol. 1989 Feb; 30(2): 109-22
AB: Plasma and erythrocyte zinc concentrations were measured in 28 Chinese pre-eclamptic women and 28 controls matched for parity, race and gestation. There were no differences in either the plasma or erythrocyte zinc concentrations between pre-eclamptic and control groups, although the mean birth weight (p less than 0.001) and period of gestation (p less than 0.001) at delivery in the control group were significantly higher. In the pre-eclamptic patients, those delivering before 37 weeks or those who gave birth to low birth weight (less than 2500 g), babies had a significantly higher plasma urate concentration (p less than 0.02) compared to the pre-eclamptic patients with better fetal outcome. However, the plasma and erythrocyte zinc concentrations between these subgroups were not significantly different. Our results suggest that zinc deficiency is unlikely to play a significant role in pre-eclampsia in our patients, and that measurement of plasma and erythrocyte zinc concentrations is of doubtful clinical value in the management of pre-eclampsia.
Record 72 of 109 in MEDLINE(R)+ (1987-1989)
TI: The effects of dietary folate and zinc on the outcome of pregnancy and early growth in rats.
AU: Fuller,-N-J; Evans,-P-H; Howlett,-M; Bates,-C-J
SO: Br-J-Nutr. 1988 Mar; 59(2): 251-9
AB: 1. The objective of the present study was to determine the effects of two levels of folic acid and two levels of zinc in the diets of rats during pregnancy and lactation. It addressed, among other things, the question of whether an inhibitory effect of folic (pteroylmonoglutamic) acid on Zn absorption might result in a secondary Zn deficiency in either the dams or the pups. 2. A purified diet was given to four groups of female DNL (Norwegian) Hooded rats, before and during pregnancy and during lactation. It contained the four possible combinations of: no added folic acid or 100 micrograms added pteroylmonoglutamic acid/g, and 6.6 or 20.2 micrograms Zn/g. Pups and dams were killed on day 20 of gestation or on day 20 postpartum. Measurements of body-weights, food intakes, blood folate and tissue Zn levels were performed. 3. The group with low Zn and low folate intake had a satisfactory reproductive outcome, and there were only minor effects of the supplements on body-weights. 4. Additional folate greatly increased blood (erythrocyte and plasma) folate levels, but did not compromise tissue Zn concentrations. Zn supplementation also enhanced blood folate levels, for reasons which are not yet clear. 5. There was a moderate enhancing effect of the Zn supplement on Zn levels in the livers and kidneys of pregnant dams, and the kidneys of lactating dams. 6. If the conclusions can be extrapolated to humans, then the results provide some reassurance that a high folate intake from prenatal supplementation need not necessarily cause Zn depletion, and hence functional Zn deficiency in pregnant women and their offspring.
Record 73 of 109 in MEDLINE(R)+ (1987-1989)
TI: Metal-binding proteins of the Syrian hamster ovaries: apparent deficiency of metallothionein.
AU: Waalkes,-M-P; Rehm,-S; Perantoni,-A
SO: Biol-Reprod. 1988 Nov; 39(4): 953-61
AB: A deficiency of metallothionein, a high-affinity metal-binding protein thought to detoxify cadmium, has been observed in rat and mouse testes, tissues that are highly susceptible to the necrotizing and carcinogenic effects of cadmium. Like the testes, the ovaries undergo a hemorrhagic necrosis when exposed to cadmium, and female Syrian hamsters have recently been shown to be highly susceptible to cadmium. However, the nature of cadmium-binding proteins in the ovary is unknown; thus, this study was undertaken to define the nature of any such proteins in the Syrian hamster ovary. A low molecular weight (Mr) zinc- and cadmium-binding protein was detected in cytosol derived from the ovaries after gel filtration that eluted with a relative elution volume similar to authentic metallothionein. This protein was extractable by heat-treatment and sequential acetone precipitation. When such extracts were further purified with a reverse phase high performance liquid chromatography (HPLC) technique developed for the isolation of metallothionein isoforms, two forms were separated. However, neither of these could be classified as metallothionein on the basis of amino acid composition, since both were particularly low in cysteine, a very common amino acid in metallothionein. The ovarian protein also contained significant amounts of aromatic amino acids, unlike metallothionein--which is devoid of aromatics, and contained much more glutamate than metallothionein. Hamsters were also made resistant to cadmium-induced ovarian necrosis by zinc treatment. Such zinc treatment, however, did not alter levels of this protein, yet caused a marked induction of hepatic metallothionein. Likewise, cadmium treatment did not increase the levels of the ovarian metal-binding protein yet markedly induced hepatic metallothionein.(ABSTRACT TRUNCATED AT 250 WORDS)
Record 74 of 109 in MEDLINE(R)+ (1987-1989)
TI: Zinc in human health and disease.
AU: Ahmad-Wahid,-M; Abdul-Hamid-Fathi,-S; Aboul-Khair,-M-R
SO: Ric-Clin-Lab. 1988 Jan-Mar; 18(1): 9-16
AB: The importance of zinc in human health and disease has been reviewed by reporting data from the recent literature. The role of zinc in human nutrition, general health, skin diseases, acrodermatitis enteropathica, reproductive physiology and pathophysiology, pregnancy, non-insulin-dependent diabetes mellitus as well as atherosclerosis is discussed. The consequences of zinc deficiency and toxicity are also illustrated.
Record 75 of 109 in MEDLINE(R)+ (1987-1989)
TI: Mobilization of tissue zinc for growth and reproduction.
SO: Nutr-Rev. 1987 Nov; 45(11): 346-8
Record 76 of 109 in MEDLINE(R)+ (1987-1989)
TI: Long-term marginal zinc deprivation in rhesus monkeys. I. Effects on adult female breeders before conception.
AU: Haynes,-D-C; Golub,-M-S; Gershwin,-M-E; Cheung,-A-T; Hurley,-L-S; Hendrickx,-A-G
SO: Am-J-Clin-Nutr. 1987 Jun; 45(6): 1492-502
AB: To assess long-term effects of marginal zinc deprivation on pregnancy, adult non-pregnant female rhesus monkeys were fed diets containing 100 or 4 ppm zinc for 1 yr. then mated; effects on pregnancy and its outcome are under study. During this year, food intake was not depressed in zinc-deprived (ZD) monkeys, and there were relatively few effects on biochemical or hematological indices. By the end of the year, plasma zinc concentration was somewhat lower in ZD monkeys than in controls. Several immune variables, including serum IgM and IgG levels and polymorphonuclear leukocyte (PMN) function, were depressed in the ZD group, changes closely reflecting circannual fluctuations in plasma zinc levels in both diet groups. Endotoxin-activated plasma from ZD monkeys had less potential to promote chemotaxis than that from control monkeys, suggesting that defective PMN function may relate to a plasma effect. Marginal zinc deprivation may thus influence immune function before other variables are affected.
CN: A100193PHS; HD14388HDNICHD; RR00169RRNCRR
Record 77 of 109 in MEDLINE(R)+ (1987-1989)
TI: Effect of zinc administration on seminal zinc and fertility of oligospermic males.
AU: Tikkiwal,-M; Ajmera,-R-L; Mathur,-N-K
SO: Indian-J-Physiol-Pharmacol. 1987 Jan-Mar; 31(1): 30-4
AB: Fourteen infertile males (age 24-45 years; married over 2 years) with idiopathic oligospermia (sperm count less than 40 millions/ml) were investigated for the effect of oral zinc sulphate (220 mg) for 4 months on their serum and seminal zinc levels, and seminal parameters. With zinc administration serum zinc levels remained essentially unaffected, however, seminal zinc levels increased significantly. There was significant improvement in sperm count, number of progressively motile and normal spermatozoa, and acid phosphates activity. Wives of 3 patients conceived. Observations suggest that zinc has potential to be used in male infertility. However, further studies are warranted.
Record 78 of 109 in MEDLINE(R)+ (1987-1989)
TI: Relationship between nutrition and reproduction in beef cattle.
SO: Vet-Clin-North-Am-Food-Anim-Pract. 1987 Nov; 3(3): 633-46
AB: The primary nutrient consideration for optimum reproductive performance in beef cattle is energy. Low energy intake delays the onset of puberty in heifers and bulls. Heifers should reach approximately 66 per cent of mature body weight by 14 to 15 months of age and be bred 30 days prior to breeding the main cow herd. Body conditioning scores (BCS) (1 = emaciated, 9 = obese) should be used to evaluate pregnant cows entering their third trimester. Cows should calve with body conditioning score 5 to 7. Forage quality and environmental factors influence maximum dry matter intake and nutrient requirements and must be considered in the clinical setting. Crude protein dietary content should be 11 to 12 per cent for lactating beef cattle. Mineral (calcium, phosphorus, magnesium, potassium, sulfur, sodium, chloride) nutrition is not a major cause of decreased reproductive performance in beef cattle. Trace mineral deficiencies (particularly selenium, copper, and zinc) can cause decreased reproductive performance. Diagnosis of these trace mineral deficiencies can be confirmed by elemental analysis of blood or tissues.
Record 79 of 109 in MEDLINE(R)+ (1981-1986)
TI: Age, sex and reproductive status alter the severity of anorexia in zinc deficient rats.
AU: Kawamoto,-J-C; Castonguay,-T-W; Keen,-C-L; Stern,-J-S; Hurley,-L-S
SO: Physiol-Behav. 1986 Oct; 38(4): 485-93
AB: Food intake and body weight gain in rats fed a zinc-deficient diet are reported. The severity of zinc deficiency-induced anorexia was observed to be dependent upon the age, sex and reproductive status of the animal. Rapidly growing rats such as weanlings, adult males, or ovariectomized females demonstrated more rapid induction of anorexia and more severe effects on cumulative food intake and body weight gain when fed zinc-deficient diets than did slowly growing (nonpregnant female adult) rats given the same diet. These results suggest that feeding in zinc-deficient animals is not regulated by dietary zinc concentration alone, but rather is mediated by one or several as yet undefined factors.
Record 80 of 109 in MEDLINE(R)+ (1981-1986)
TI: Serum and semen zinc levels in normozoospermic and oligozoospermic men.
AU: Madding,-C-I; Jacob,-M; Ramsay,-V-P; Sokol,-R-Z
SO: Ann-Nutr-Metab. 1986; 30(4): 213-8
AB: Zinc is necessary for growth, sexual maturation and reproduction. Because high concentrations of zinc are found in the male reproductive system, a relationship between zinc and male infertility has been suggested. We studied 11 unselected men who presented to a Reproductive Endocrinology Clinic with histories of infertility and low sperm counts. Reproductive hormones and semen and serum zinc levels were measured. All men had semen analyses performed on at least three separate occasions. A similar set of laboratory evaluations were performed on 11 other men who had normal semen analyses and no history of infertility. No abnormalities of reproductive hormones were found in either group. Mean serum zinc levels were significantly lower in the infertile men (p less than 0.05). Mean semen zinc levels were not significantly different. There was no correlation between serum and semen zinc levels in either group. A significant correlation was found between sperm count and semen zinc (r = 0.66, p less than 0.05) in the volunteers with normal counts, but not in the oligozoospermic men. The results obtained in this study suggest that lowered serum zinc is more common than formerly appreciated in unselected patients with infertility. The high level of zinc found in semen is due primarily to the secretions of the prostate gland and reflects prostatic stores. Serum zinc is thought to be a reasonable indicator of zinc status. The lack of correlation between serum zinc and semen zinc found in our study suggests that mild zinc deficiency may lower serum zinc while the larger prostatic zinc stores remain unaffected.(ABSTRACT TRUNCATED AT 250 WORDS)
CN: 5T32AM07214AMNIADDK; RR00425RRNCRR
Record 81 of 109 in MEDLINE(R)+ (1981-1986)
TI: Clinical and biochemical manifestations of zinc deficiency in human subjects.
SO: J-Am-Coll-Nutr. 1985; 4(1): 65-72
AB: During the past two decades, essentiality of zinc for man has been established. Deficiency of zinc in man attributable to nutritional factors and several diseased states has been recognized. High phytate content of cereal proteins decreases availability of zinc; thus the prevalence of zinc deficiency is likely to be high in the population subsisting mainly on cereal proteins. Zinc deficiency has been noted to occur in patients with malabsorption syndrome, chronic renal disease, cirrhosis of the liver, sickle cell disease, AE (acrodermatitis enteropathica), and other chronically debilitating diseases. Growth retardation, male hypogonadism, skin changes, poor appetite, mental lethargy, and delayed wound healing are some of the manifestations of chronically zinc-deficient human subjects. In severely zinc-deficient patients, dermatological manifestations, diarrhea, alopecia, mental disturbances, and intercurrent infections predominate. If untreated, the condition becomes fatal. Zinc deficiency affects testicular functions adversely in man and animals. This effect of zinc is at the end-organ level. It appears that zinc is essential for spermatogenesis. Zinc is involved in many biochemical functions. Several zinc metalloenzymes have been recognized in the past decade. Zinc is required for each step of cell cycle in microorganisms and is essential for DNA synthesis. The effect of zinc on protein synthesis may be attributable to its vital role in nucleic acid metabolism. The activities of many zinc-dependent enzymes have been shown to be affected adversely in zinc-deficient tissues.(ABSTRACT TRUNCATED AT 250 WORDS)
Record 82 of 109 in MEDLINE(R)+ (1981-1986)
TI: Clinical and biochemical manifestation zinc deficiency in human subjects.
SO: J-Pharmacol. 1985 Oct-Dec; 16(4): 344-52
AB: During the past two decades, essentiality of zinc for man has been established. Deficiency of zinc in man attributable to nutritional factors and several diseased states has been recognized. High phytate content of cereal proteins decreases availability of zinc, thus the prevalence of zinc deficiency is likely to be high in the population subsisting on cereal proteins mainly. Zinc deficiency has been noted to occur in patients with malabsorption syndrome, chronic renal disease, cirrhosis of the liver, sickle cell disease, AE, and other chronically debilitating diseases. Growth retardation, male hypogonadism, skin changes, poor appetite, mental lethargy and delayed wound healing are some of the manifestations of chronically zinc-deficient human subjects. In severely zinc-deficient patients, dermatological manifestations, diarrhea, alopecia, mental disturbances and intercurrent infections predominate. If untreated, the condition becomes fatal. Zinc deficiency affects testicular functions adversely in man and animals. This effect of zinc is at the end-organ level. It appears that zinc is essential for spermatogenesis. Zinc is involved in many biochemical functions. Several zinc metalloenzymes have been recognized in the past decade. Zinc is required for each step of cell cycle in microorganisms and is essential for DNA synthesis. The effect of zinc on protein synthesis may be attributable to its vital role in nucleic acid metabolism. The activities of many zinc-dependent enzymes have been shown to be affected adversely in zinc-deficient tissues. Zinc atoms in some of the enzyme molecules participate in catalysis and also appear to be essential for maintenance of structure of apoenzymes. Zinc also plays a role in stabilization of biomembrane structure and polynucleotide confirmation.(ABSTRACT TRUNCATED AT 250 WORDS)
Record 83 of 109 in MEDLINE(R)+ (1981-1986)
TI: Effect on the ewe and lamb of low zinc intake throughout pregnancy.
AU: Apgar,-J; Fitzgerald,-J-A
SO: J-Anim-Sci. 1985 Jun; 60(6): 1530-8
AB: Throughout pregnancy, 30 primiparous Finn cross ewes were given a low Zn (less than or equal to 1 ppm) semi-purified diet. A 100-g hay supplement was fed three to seven times/week. Supplemental Zn (20 ppm) was provided in the drinking water of 14 ewes. At parturition, lambs were removed from ewes before suckling. Viable lambs not taken for tissue analysis were given 200 ml cow colostrum and raised on an artificial feeder. Throughout gestation, unsupplemented (-Zn) ewes gained less weight and had lower plasma Zn levels than Zn-supplemented (+Zn) ewes. One -Zn ewe was not pregnant, three aborted, one resorbed, one delivered mummified twins at term and two delivered malformed lambs. Average weight of lambs born to -Zn ewes d 136 or later (excluding mummified twins and one weighing less than 20% as much as its twin) was 1.8 +/- .6 (SE) kg. Only three lambs born to -Zn ewes were vigorous enough to put on the artificial feeder; none survived. One +Zn ewe was not pregnant. Of 23 lambs born to the remaining +Zn ewes, five were used for tissue analysis, two lambs of triplets were born dead, twins born d 138 died at birth. One twin died 6 d after birth. The 14 remaining lambs were weaned in good health. Average birth weight of +Zn lambs was 3.3 +/- 1.0 kg. Increased salivation was seen in -Zn ewes after 6 wk of low Zn intake.(ABSTRACT TRUNCATED AT 250 WORDS)
Record 84 of 109 in MEDLINE(R)+ (1981-1986)
TI: Clinical, endocrinological and biochemical effects of zinc deficiency.
SO: Clin-Endocrinol-Metab. 1985 Aug; 14(3): 567-89
AB: The essentiality of zinc for humans was recognized in the early 1960s. The causes of zinc deficiency include malnutrition, alcoholism, malabsorption, extensive burns, chronic debilitating disorders, chronic renal disease, certain diuretics, the use of chelating agents such as penicillamine for Wilson's disease, and genetic disorders such as acrodermatitis enteropathica and sickle cell disease. The requirement of zinc is increased in pregnancy and during the growing age period. The clinical manifestations in severe cases of zinc deficiency included bullous-pustular dermatitis, alopecia, diarrhoea, emotional disorder, weight loss, intercurrent infections, hypogonadism in males and it is fatal if untreated. A moderate deficiency of zinc is characterized by growth retardation and delayed puberty in adolescents, hypogonadism in males, rough skin, poor appetite, mental lethargy, delayed wound healing, taste abnormalities and abnormal dark adaptation. In mild cases of zinc deficiency in human subjects, we have observed oligospermia, slight weight loss and hyperammonaemia. Zinc is a growth factor. As a result of its deficiency, growth is affected adversely in many animal species and in man. Inasmuch as zinc is needed for protein and DNA synthesis and cell division, it is believed that the growth effect of zinc is related to its effect on protein synthesis. Testicular functions are affected adversely as a result of zinc deficiency in both humans and experimental animals. This effect of zinc is at the end organ level and the hypothalamic--pituitary axis is intact in zinc-deficient subjects. Inasmuch as zinc is intimately involved in a cell division, its deficiency may adversely affect testicular size and thus its function. In mice, the incidence of degenerate oocytes, and hypohaploidy and hyperhaploidy in metaphase II oocytes were increased due to zinc deficiency. Zinc at physiological concentrations reduced prolactin secretion from the pituitary in vitro and it has been suggested that this trace element may have a role in the in vivo regulation of prolactin release. Thymopoietin, a hormone needed for T-cell maturation, has also been shown to be zinc dependent. It is clear that zinc may have several roles in biochemical and hormonal functions of various endocrine organs. Future research in this area is very much needed.
Record 85 of 109 in MEDLINE(R)+ (1981-1986)
TI: Zinc deficiency in pregnant Long-Evans hooded rats: teratogenicity and tissue trace elements.
AU: Rogers,-J-M; Keen,-C-L; Hurley,-L-S
SO: Teratology. 1985 Feb; 31(1): 89-100
AB: The Long-Evans hooded rat is widely used in experimental teratology. This study determines the teratogenicity of maternal Zn deficiency in the Long-Evans hooded rat, and examines the effects of Zn deficiency on Zn, Fe, and Cu concentrations in maternal and fetal tissues. Dams were fed an egg white-based diet containing 100 micrograms/g Zn for 1 week prior to mating. At mating rats were fed diets with 0.5, 4.5, 9.0, or 100 micrograms/g Zn ad lib, or 100 micrograms/g Zn pair-fed to 0.5 micrograms/g Zn dams. Laparotomies were performed on day 21 of gestation. Live fetuses and resorptions were counted. Fetuses were weighed and examined for external malformations. Some fetuses were used for Zn, Fe, and Cu determinations, others for internal or skeletal examination. Zn, Fe, and Cu levels were determined in maternal liver, kidney, and plasma. The 0.5 micrograms/g Zn dams lost weight during pregnancy; 27% of implantation sites were resorbed, 91.7% of live fetuses were malformed, and fetal weight was low. There were no malformed fetuses in the 4.5 micrograms/g Zn or 9.0 micrograms/g Zn groups; litter weights were low in the 4.5 micrograms/g Zn group. Tissue Zn was correlated with dietary Zn. Increased Fe concentration occurred in all maternal and fetal tissues in the 0.5 micrograms/g Zn group. The teratogenicity of Zn deficiency in the Long-Evans rat appears similar to that previously reported in the Sprague-Dawley strain.
CN: EY05657EYNEI; HD01743HDNICHD
Record 86 of 109 in MEDLINE(R)+ (1981-1986)
TI: Zinc and reproduction.
SO: Annu-Rev-Nutr. 1985; 543-68
Record 87 of 109 in MEDLINE(R)+ (1981-1986)
TI: Studies of marginal zinc deprivation in rhesus monkeys: II. Pregnancy outcome.
AU: Golub,-M-S; Gershwin,-M-E; Hurley,-L-S; Baly,-D-L; Hendrickx,-A-G
SO: Am-J-Clin-Nutr. 1984 Jun; 39(6): 879-87
AB: A marginal state of zinc deficiency was induced in the pregnant nonhuman primate, Macaca mulatta, by feeding a diet containing 4 ppm zinc beginning at conception. Pregnancy outcome of marginally zinc-deficient monkeys (ZD) was compared to both pair-fed (PF) and ad libitum fed (AL) control animals (100 ppm zinc). Stillbirths, abortions, and delivery complications were more frequent in both ZD and PF dams than in AL controls; no malformations were detected (maternal plasma zinc was normal during organogenesis). Male ZD neonates weighed significantly less than same sex controls; also, in relation to colony norms, 7/8 ZD males, 2/8 ZD females, and 1/10 PF controls were of low birth weight. Further, plasma zinc and iron levels were lower in ZD neonates than in AL and PF controls. ZD neonates also had reduced muscle tonus. Birth weight and maternal plasma zinc concentration were negatively correlated in ZD group but positively correlated in AL and PF groups. Indeed, maternal plasma zinc concentration alone did not identify a state of zinc deficiency which impaired fetal growth in monkeys.
CN: AI00193AINIAID; HD14388HDNICHD; RR00169RRNCRR
Record 88 of 109 in MEDLINE(R)+ (1981-1986)
TI: Response of the reproductive system of male rats to protein and zinc deficiency during puberty.
AU: Salem,-S-I; Coward,-W-A; Lunn,-P-G; Hudson,-G-J
SO: Ann-Nutr-Metab. 1984; 28(1): 44-51
AB: Male weanling rats were fed four diets providing high or low levels of protein and/or zinc. One group on each diet was sacrificed every 2 weeks to measure the weights of the reproductive organs, plasma levels of follicle-stimulating hormone and luteinizing hormone, and the plasma and testicular concentrations of testosterone, dihydrotestosterone and zinc. The results demonstrate that hypogonadal states are produced in response to protein deficiency and zinc deficiency but the mechanisms involved are different. The specific effects of zinc deficiency are not observed in protein-deficient animals.
Record 89 of 109 in MEDLINE(R)+ (1981-1986)
TI: Nutrition and the pill.
SO: J-Reprod-Med. 1984 Jul; 29(7 Suppl): 547-50
AB: Apart from their gynecologic influence as birth control agents, oral contraceptives (OCs) have been shown to affect a number of metabolic and nutritional processes, some insignificantly and others beneficially. The use of contraceptive pills has been shown to decrease the physiologic levels of six nutrients--riboflavin, pyridoxine, folacin, vitamin B12, ascorbic acid and zinc--and to increase the levels of four others--vitamin C, iron, copper and vitamin A. Women who take OCs and have adequate diets need little or no supplemental vitamins. Vitamin and mineral increases caused by OCs do not require treatment.
Record 90 of 109 in MEDLINE(R)+ (1981-1986)
TI: Studies of marginal zinc deprivation in rhesus monkeys. V. Fetal and infant skeletal effects.
AU: Leek,-J-C; Vogler,-J-B; Gershwin,-M-E; Golub,-M-S; Hurley,-L-S; Hendrickx,-A-G
SO: Am-J-Clin-Nutr. 1984 Dec; 40(6): 1203-12
AB: Skeletal maturation was evaluated in newborn and infant rhesus monkeys that had been subjected to a marginally zinc-deficient diet (4 ppm zinc) from conception through 12 months of postnatal life. Serial radiographic assessment of skeletal development was performed and compared to both ad libitum and pair-fed controls. Radiographs were obtained at birth and at 1, 3, 9, and 12 months of age. In each age group a maturation indicator was selected to identify individuals with abnormal skeletal maturation defined on the basis of presence of epiphyseal ossification centers. Animals were compared only within a given sex group. Additionally, to evaluate endochondral bone mineralization, the appearance of the zone of provisional calcification on the metaphyseal side of the growth plate and the width of the growth plate were assessed. A marginal level of zinc deprivation during gestation and during the 1st yr of life was found to be associated with significantly delayed skeletal maturation and defective mineralization. This abnormality of bone mineralization has many features similar to human rachitic syndromes and suggests that zinc plays an important role in endochondral bone formation.
CN: AI00193AINIAID; HD14388HDNICHD; RR00169RRNCRR
Record 91 of 109 in MEDLINE(R)+ (1981-1986)
TI: Zinc in mammalian sperm: a review.
AU: Hidiroglou,-M; Knipfel,-J-E
SO: J-Dairy-Sci. 1984 Jun; 67(6): 1147-56
AB: The relationship of zinc to morphologic, physiologic, and metabolic functions in the male reproductive system are summarized, and gaps in current understanding are pointed out. Semen and its constituents generally contain high zinc, although concentrations vary among animals and species; the relationships between zinc and fertility of semen is unclear. During zinc deficiency, retarded development of testicular growth involved marked atrophy of tubular epithelium and reduced deoxyribonucleic acid, ribonucleic acid, and protein, as well as reduced zinc contents of testis, epididymis, and dorsolateral prostate. Functions of zinc in hormone interrelationships are little understood, but zinc deficiency decreases output of pituitary gonadotrophins and androgen production, and zinc turnover involves testosterone as well as pituitary hormones. Metabolic regulation of sperm appears to be mediated through zinc as a regulator of enzyme activity in the semen. Within spermatozoa, zinc is closely associated with sulfhydryl groups and disulfide linkages and is concentrated in the tail. Control of motility of sperm by zinc apparently involves control of energy utilization through adenosine triphosphate systems involved in contraction and through regulation of phospholipid energy reserves. The many roles for zinc in the male reproductive system are extremely complex and scarcely understood. The importance of zinc contents of commonly utilized feedstuffs in relation to reproductive capabilities of the mammalian sperm remain unclear, although zinc deficiency in relation to male reproduction may be much more widespread than is recognized commonly.
Record 92 of 109 in MEDLINE(R)+ (1981-1986)
TI: Zinc deficiency teratogenicity: the protective role of maternal tissue catabolism.
AU: Masters,-D-G; Keen,-C-L; Lonnerdal,-B; Hurley,-L-S
SO: J-Nutr. 1983 Apr; 113(4): 905-12
AB: The effect of maternal metabolic state on the response to dietary zinc deficiency was assessed with the pregnant rat as a model. Sprague-Dawley rats were fed from mating to term: 1) a zinc-adequate (100 micrograms/g) control diet ad libitum, or 2) a zinc-deficient diet (0.7 micrograms/g) ad libitum, or 3) a control diet at reduced intake, or 4) a zinc-deficient diet at reduced intake, or 5) a zinc-deficient diet ad libitum plus additional zinc-deficient diet, fed by intubation, to maintain total intake at approximately 14 g/day. Dams receiving the zinc-deficient diet deposited more zinc (240-330%) into the products of conception than was consumed, showing that tissue catabolism is a substantial source of zinc. In rats fed the control diet ad libitum only 3% of the zinc consumed was deposited into the products of conception. Litters from dams fed the deficient diet at restricted levels (resulting in greater tissue catabolism) had fewer malformations and resorptions than litters from dams fed the zinc-deficient diet ad libitum. Maintenance of total intake of the zinc-deficient diet at 14 g/day by intubation resulted in a pronounced drop in voluntary intake. By day 18 of pregnancy voluntary intake had almost ceased, following day 18 the rats became severely distressed if any zinc-deficient diet was force-fed. Rats fed the zinc-deficient diet ad libitum also displayed a dramatic fall in voluntary intake after day 18 of gestation. These data show that the reduction in food intake during zinc deficiency is not due to gustatory influences alone and that metabolic state, defined as the balance between anabolism and catabolism, is a critical factor in determining the availability of zinc to the litter during zinc deficiency.
Record 93 of 109 in MEDLINE(R)+ (1981-1986)
TI: Plasma levels of prostaglandin metabolites in zinc-deficient female rats near term.
AU: O'Dell,-B-L; Browning,-J-D; Reeves,-P-G
SO: J-Nutr. 1983 Apr; 113(4): 760-5
AB: To investigate the possibility that impaired prostaglandin biosynthesis is involved in the development of postpartum illness in zinc-deficient female rats, plasma levels of three prostaglandin metabolites, 13,14-dihydro-15-keto PGF2 alpha, 13,14-dihydro-15-keto PGE2, and 6-keto PGF1 alpha were determined on day 22 of gestation. During the gestation period female rats were fed low zinc (less than 1 ppm) diets based on soybean protein or similar control diets (100 ppm Zn). Two levels of vitamin E, 15 and 65 IU per kilogram, were added to the diet. Zinc deficiency in dams fed the diet containing 65 IU/kg vitamin E resulted in significantly higher plasma levels of 13,14-dihydro-15-keto PGF2 alpha than controls; plasma 6-keto PGF1 alpha levels were not different. Zinc-deficient dams fed the basal diet containing 15 IU/kg vitamin E had significantly higher plasma levels of all three prostaglandin metabolites than controls. The pathology of zinc deficiency is not due to decreased prostaglandin production, but the present results and the pathological signs are consistent with failure of prostaglandin function.
Record 94 of 109 in MEDLINE(R)+ (1981-1986)
TI: Zinc deficiency in human subjects.
SO: Prog-Clin-Biol-Res. 1983; 1291-33
AB: During the past two decades, the essentiality of zinc for man has been established. Deficiency of zinc in man due to nutritional factors and several diseased states has been recognized. High phytate content of cereal proteins decreases availability of zinc; thus the prevalence of zinc deficiency is likely to be high in a population subsisting mainly on cereal proteins. Alcoholism is known to cause hyperzincuria and thus may play a role in producing zinc deficiency in man. Malabsorption, cirrhosis of the liver, chronic renal disease and other chronically debilitating diseases may similarly induce zinc deficiency in human subjects. A severe deficiency of zinc has recently been recognized to occur in patients with sickle cell anemia and a beneficial effect of zinc therapy in such patients has been reported. Growth retardation, male hypogonadism, skin changes, poor appetite, mental lethargy and delayed wound healing are some of the manifestations of chronically zinc-deficient human subjects. Taste abnormalities, correctable with zinc supplementation, have been observed in uremic subjects. Recently, abnormal dark adaptation related to zinc deficiency in patients with cirrhosis of the liver and sickle cell disease has been reported. In severely zinc-deficient patients, dermatological manifestations, diarrhea, alopecia, mental disturbances and intercurrent infections predominate and if untreated the condition becomes fatal. Zinc deficiency is known to affect testicular functions adversely in man and animals. This effect of zinc is at the end organ level and it appears that zinc is essential for spermatogenesis and testosterone steroidogenesis. Zinc is involved in many biochemical functions. Several zinc metalloenzymes have been recognized in the past decade. Zinc is required for each step of cell cycle in microorganisms and is essential for DNA synthesis. Thymidine kinase, RNA polymerase, DNA-polymerase from various sources and RNA-dependent DNA polymerase from viruses have been shown to be zinc-dependent enzymes. Zinc also regulates the activity of RNase; thus the catabolism of RNA appears to be zinc-dependent. The effect of zinc on protein synthesis may be attributable to its vital role in nucleic acid metabolism. The activities of many zinc-dependent enzymes have been shown to be affected adversely in zinc-deficient tissues. Three enzymes, alkaline phosphatase, carboxypeptidase and thymidine kinase, appear to be most sensitive to zinc restriction in that their activities are affected adversely within three to six days of institution of a zinc-deficient diet to experimental animals.(ABSTRACT TRUNCATED AT 400 WORDS)
Record 95 of 109 in MEDLINE(R)+ (1981-1986)
TI: Comparative aspects of dietary copper and zinc deficiencies in pregnant rats.
AU: Masters,-D-G; Keen,-C-L; Lonnerdal,-B; Hurley,-L-S
SO: J-Nutr. 1983 Jul; 113(7): 1448-51
AB: The utilization and distribution of copper during dietary copper deficiency was studied in the pregnant rat, and the effects of maternal copper deficiency on fetal development were compared with those of maternal zinc deficiency. Sprague-Dawley rats were fed from mating to term (per gram diet): 1) a control diet (10 micrograms copper, 100 micrograms zinc) or 2) a copper-deficient diet (0.7 micrograms copper, 100 micrograms zinc) or 3) a zinc-deficient diet (10 micrograms copper; 0.7 micrograms zinc). Dams fed the copper-deficient diet deposited only 15.5% of the dietary copper consumed during pregnancy into the products of conception (fetuses, uterus and placentas); in comparison dams fed the zinc-deficient diet deposited more zinc into their litters than was consumed (240%). Copper concentration in the fetuses of copper-deficient dams was 30% of that of controls, but the size and number of live fetuses was unaffected. The zinc concentration of the zinc-deficient fetuses was 78% of that of the controls, and both the size and number of live fetuses were considerably lower than normal. Accumulation of copper in the products of conception may be accounted for by dietary copper intake, whereas accumulation of zinc in fetuses of zinc-deficient females is dependent in part on catabolism of maternal tissues.
Record 96 of 109 in MEDLINE(R)+ (1981-1986)
TI: Concentrations of morphologically normal, motile spermatozoa: Mg, Ca and Zn in the semen of infertile men.
AU: Pandy,-V-K; Parmeshwaran,-M; Soman,-S-D; Dacosta,-J-C
SO: Sci-Total-Environ. 1983 Mar; 27(1): 49-52
AB: Semen from infertile men (n = 23) has been compared with that of control subjects (n = 25). Whereas the concentrations of morphologically normal, motile sperms, Mg, Ca and Zn fell within the acceptable limits for all the control subjects, only two infertile men qualified by all five parameters. Of the patient group, seven were abnormal on all counts; sperm motility, Mg and Zn were low in 16, Ca in 19 and abnormal morphology was encountered in 12. Since there was no linear correlation between any two parameters, it is possible that each factor may singly or jointly influence the physiological integrity of the spermatozoa. The results are discussed from a consideration of pathological manifestations known to occur in deficiency of these trace elements a propos their role in determining the fertility index of the semen.
Record 97 of 109 in MEDLINE(R)+ (1981-1986)
TI: Effect of oral zinc therapy on gonadal function in hemodialysis patients. A double-blind study.
AU: Mahajan,-S-K; Abbasi,-A-A; Prasad,-A-S; Rabbani,-P; Briggs,-W-A; McDonald,-F-D
SO: Ann-Intern-Med. 1982 Sep; 97(3): 357-61
AB: Zinc deficiency may account for the persistence of gonadal dysfunction in a majority of uremic men despite adequate dialysis. Twenty stable patients having hemodialysis three times a week completed a double-blind trial using either 50 mg of elemental zinc as zinc acetate (10 patients) or placebo (10 patients), orally. At the end of the 6-month study period, a significant increase in the mean (+/- SE) plasma zinc (75 +/- 2 micrograms/dL to 100 +/- 2 micrograms/dL, p less than 0.001), serum testosterone (2.8 +/- 0.3 ng/dL to 5.2 +/- 0.5 ng/mL, p less than 0.001), and sperm count (30 +/- 3 million/mL to 63 +/- 5 million/mL, p less than 0.001) occurred in the zinc-treated group, but not in those receiving the placebo. The zinc-treated group also had a significant fall in serum luteinizing hormone (92 +2- 10 mIU/mL to 49 +/- 26 mIU/mL, p less than 0.005) and follicle stimulating hormone (45 +/- 9 mIU/mL to 25 +/- 7 mIU/mL, p less than 0.05), not seen in the placebo group. Patients receiving zinc had an improvement in potency, libido, and frequency of intercourse not found in the placebo group. These results suggest that zinc deficiency is a reversible cause of gonadal dysfunction in patients having regular hemodialysis.
Record 98 of 109 in MEDLINE(R)+ (1981-1986)
TI: Testicular damage associated with zinc deficiency in pre- and postpubertal rats: response to zinc repletion.
AU: Mason,-K-E; Burns,-W-A; Smith,-J-C
SO: J-Nutr. 1982 May; 112(5): 1019-28
Record 99 of 109 in MEDLINE(R)+ (1981-1986)
TI: Plasma zinc in hypertension/toxemia and other reproductive variables in adolescent pregnancy.
AU: Cherry,-F-F; Bennett,-E-A; Bazzano,-G-S; Johnson,-L-K; Fosmire,-G-J; Batson,-H-K
SO: Am-J-Clin-Nutr. 1981 Nov; 34(11): 2367-75
AB: A study was conducted at Charity Hospital, New Orleans, among 272 adolescent pregnant women to ascertain the relationship of pregnancy outcome to plasma zinc level measured once at the time of enrollment. Regression analyses were performed on zinc status versus parameters concerning success of pregnancy corrected for gestational stage at specimen collection. Analysis of variance was performed on groups according to presence or absence of complications, with analyses of covariance used to analyze dichotomous groups. Low, though widely variable, plasma zinc levels were found (mean = 58 +/- 12.6 micrograms/dl). Zinc values differed significantly by gestational stage at collection, the regression coefficient indicating a decline of 0.07 micrograms/dl/day. Plasma zinc level correlated significantly with Hb, red blood cells, ferritin, and folic acid. As to course of pregnancy, women experiencing hypertension/toxemia were found to have significantly lower plasma zinc level. Among infants displaying congenital defects at birth those with undescended testes and metatarsus varus were delivered by mothers whose plasma zinc was well below the mean for the group. These findings indicate the need to investigate the influence of dietary patterns and zinc intake on maternal plasma zinc level and pregnancy outcome, further delineating the role of zinc in human reproduction, particularly hypertension of pregnancy.
Record 100 of 109 in MEDLINE(R)+ (1981-1986)
TI: Zinc deficiency in the cat.
AU: Kane,-E; Morris,-J-G; Rogers,-Q-R; Ihrke,-P-J; Cupps,-P-T
SO: J-Nutr. 1981 Mar; 111(3): 488-95
AB: Two experiments were conducted to produce Zn deficiency in, and to establish approximate Zn requirements of, the cat. In experiment 1, soy protein (SP)-based diets were fed for 8 months: diet 1, basal, without added Zn, 15 ppm; diet 2, basal, 15 ppm Zn plus 2% CaHPO4; and diet 3, basal with added Zn, 67 ppm. Gross Zn deficiency symptoms were not observed, although spermatogenesis in cats fed diets 1 and 2 was abnormal. There were no differences in food intake or growth rate between treatments. Mean plasma zinc levels (micrograms/100 ml) for cats fed diets 1, 2 and 3 were 55, 47 and 89, respectively. In experiment 2, the SP was washed with EDTA. Ten 8-week-old kittens were fed the following diets for 14 weeks: diet 4, SP without Zn, 0.7 ppm Zn; diet 5, containing 52 ppm Zn; or diet 6, an amino acid diet, 4.8 ppm Zn. Mean food intake (g/day) and weight gains (g/day) for cats fed diets 4, 5 and 6 were: 17.2, 0.4; 55.0, 19.5; and 31.5, 10.0, respectively. Mean plasma Zn levels (micrograms/100 ml) and liver Zn (ppm) for cats fed diet 4 had poor coats characterized by thinning and slow hair growth and scaliness of the skin and ulcerations of the buccal margins. The cat's requirement for zinc is probably between 15 ppm and 50 ppm.
Record 101 of 109 in MEDLINE(R)+ (1975-1980)
TI: Relation of mammalian sperm chromatin heterogeneity to fertility.
AU: Evenson,-D-P; Darzynkiewicz,-Z; Melamed,-M-R
SO: Science. 1980 Dec 5; 210(4474): 1131-3
AB: Flow cytometry of heated sperm nuclei revealed a significant decrease in resistance to in situ denaturation of spermatozoal DNA in samples from bulls, mice, and humans of low or questionable fertility when compared with others of high fertility. Since thermal denaturation of DNA in situ depends on chromatin structure, it is assumed that changes in sperm chromatin conformation may be related to the diminished fertility. Flow cytometry of heated sperm nuclei may provide a new and independent determinant of male fertility.
Record 102 of 109 in MEDLINE(R)+ (1975-1980)
TI: Ultrastructural changes in the sperm-tail of zinc-deficient rats.
AU: Dinsdale,-D; Williams,-R-B
SO: J-Comp-Pathol. 1980 Oct; 90(4): 559-66
Record 103 of 109 in MEDLINE(R)+ (1975-1980)
TI: Experimental zinc deficiency in man. Effect on testicular function.
AU: Abbasi,-A-A; Prasad,-A-S; Rabbani,-P; DuMouchelle,-E
SO: J-Lab-Clin-Med. 1980 Sep; 96(3): 544-50
AB: Dietary zinc intake was restricted (2.7 to 5.0 mg daily) for 24 to 40 weeks in five male volunteers. Their mean age was 57 years. Oligospermia (total sperm count less than 40 million per ejaculate) was induced in four out of five subjects. A decrease in the sperm count occurred during zinc restricion and the early phase of zinc repletion before body stores of zinc were restored to normal. The duration of oligospermia in the four subjects ranged from 6 to 14 months. Oligospermia was reversed after zinc supplementation in physiologic amounts. The baseline sperm concentration and total sperm count per ejaculate in all five subjects dropped significantly (p < 0.05) after zinc restriction and returned to normal 6 to 12 months after zinc supplementation. The decrease in sperm count coincided with decline in Leydig cell function and was reversed after zinc supplementation in low doses. Our study has demonstrated that dietary restriction of zinc can affect testicular function adversely. This effect of zinc deficiency, however, is a reversible process and can be corrected by proper supplementation with zinc.
Record 104 of 109 in MEDLINE(R)+ (1975-1980)
TI: Zinc deficiency in rhesus and bonnet monkeys, including effects on reproduction.
AU: Swenerton,-H; Hurley,-L-S
SO: J-Nutr. 1980 Mar; 110(3): 575-83
AB: Zinc deficiency was induced in two species of monkeys, Macaca mulatta (rhesus) and Macaca radiata (bonnet), by feeding a purified diet containing isolated soybean protein. In both rhesus and bonnet monkeys, plasma zinc levels were reduced in 7 or 14 days after institution of the zinc-deficiency regimen. Dermal lesions on the extremities, face and abdomen, and alopecia also appeared in both species. Reduced hair zinc concentration was observed in zinc-deficient bonnet monkeys. Oral supplementation with zinc rapidly reversed the dermal lesions and hair loss of deficient monkeys, however, repleted monkeys still had lower hair zinc levels than controls. Normal reproduction was impaired when the zinc-deficient diet was fed to adult monkeys. In pregnant rhesus monkeys, one zinc-deficient monkey aborted on day 48 of pregnancy. Under other experimental conditions, fetuses removed by cesarean section on day 70 or 100 of pregnancy did not show gross congenital abnormalities. In zinc-deficient bonnet monkeys, none of the matings resulted in pregnancies, and after prolonged deficiency menstrual cycles ceased together. The zinc-supplemented control diet supported normal reproduction.
Record 105 of 109 in MEDLINE(R)+ (1975-1980)
TI: Trace element deficiencies and fertility in ruminants: a review.
SO: J-Dairy-Sci. 1979 Aug; 62(8): 1195-206
AB: Various minerals (copper, cobalt, selenium, manganese, iodine, zinc, and iron) can influence reproductive performance of ruminants. Reproductive failure may be induced by deficiencies of single or combined trace elements and by imbalances. This review is focused on maladjustments of trace elements leading to impaired breeding performance. Opinion is diverse as to the existence of various reproductive disturbances from either a severe copper depletion or a marginal dietary copper deficiency. Field experience suggests that administration of cobalt to ruminants on cobalt-deficient diets improves their impaired breeding performance. Selenium infertility in ewes is more prevalent in some areas and in some seasons, but the actual cause of this malady and the continuing role of additional factors are unknown. Manganese is necessary for normal fertility in ruminants, and feeding low-manganese rations depresses conception rates. Lack of iodine impairs thyroid activity and also ovarian function. Reproductive failure in the female and in spermatogenesis are manifestations of zinc deficiency. Despite forages rich in iron, low availability in certain instances could affect adversely ruminant reproduction. Knowledge of biochemical dysfunctions from trace element deficiencies is essential to determine the role which trace elements play in fertility of ruminant animals.
Record 106 of 109 in MEDLINE(R)+ (1975-1980)
TI: Beneficial effect of zinc supplementation on reproduction in rats fed rapeseed protein concentrate.
AU: Shah,-B-G; Giroux,-A; Belonje,-B; Jones,-J-D
SO: Nutr-Metab. 1979; 23(4): 275-85
AB: Three groups of 33 90-day-old female Sprague-Dawley rats were fed, ad libitum, the following diets for 2 weeks before breeding. Diet 1 (D1) contained 20% protein from casein, diet 2 (D2) had the same level of protein from Tower rapeseed (Brassica napus) protein concontrate (RPC) and diet 3 (D3) was the same as D2 with a zinc supplement (70 mg/l) in the drinking water. From each group 6 animals were killed before breeding and 5-9 animals were killed at 1 and 2 weeks of gestation and post-partum. From each rat, blood, thyroids, liver and femur were collected for the determination of zinc, copper, iron, manganese, calcium and magnesium. As a measure of the reproductive performance, body weight, number of pups in the uterus or delivered live or dead, and gestations days before parturition were recorded. The pups were examined for obvious deformities and also analysed for the above mineral elements by atomic absorption spectroscopy. In group D2, levels of zinc in maternal serum, liver, femur and in the pups were significantly lower than the comparable levels in the other two groups. The zinc supplemented RPC-fed group did not show the anorexia experienced by the unsupplemented group and there was neither a significant difference between reproductive performances of groups D1 and D3 nor was there any significant difference between the zinc levels determined. It was concluded that the toxic symptoms caused by RPC feeding was attributable to zinc deficiency probably caused by the high phytate level in the RPC.
Record 107 of 109 in MEDLINE(R)+ (1975-1980)
TI: Beneficial effect of zinc supplementation on reproduction in rats red rapeseed protein concentrate.
AU: Shah,-B-G; Giroux,-A; Belonje,-B; Jones,-J-D
SO: Nutr-Metab. 1979; 23(4): 275-85
AB: Three groups of 33 90-day-old female Sprague-Dawley rats were fed, ad libitum, the following diets for 2 weeks before breeding. Diet 1 (D1) contained 20% protein from casein, diet 2 (D2) had the same level of protein from Tower rapeseed (Brassica napus) protein concontrate (RPC) and diet 3 (D3) was the same as D2 with a zinc supplement (70 mg/l) in the drinking water. From each group 6 animals were killed before breeding and 5--9 animals were killed at 1 and 2 weeks of gestation and post-partum. From each rat, blood, thyroids, liver and femur were collected for the determination of zinc, copper, iron, manganese, calcium and magnesium. As a measure of the reproductive performance, body weight, number of pups in the uterus or delivered live or dead, and gestation days before parturition were recorded. The pups were examined for obvious deformities and also analyzed for the above mineral elements by atomic absorption spectroscopy. In group D2, levels of zinc in maternal serum, liver, femur and in the pups were significantly lower than the comparable levels in the other two groups. The zinc supplemented RPC-fed group did not show the anorexia experienced by the unsupplemented group and there was neither a significant difference between reproductive performances of groups D1 and D3 nor was there any significant difference between the zinc levels determined. It was concluded that the toxic symptoms caused by RPC feeding were attributable to zinc deficiency probably caused by the high phytate level in the RPC.
Record 108 of 109 in MEDLINE(R)+ (1975-1980)
TI: Experimental zinc deficiency in man: effect on spermatogenesis.
AU: Abbasi,-A-A; Prasad,-A-S; Rabbani,-P-R
SO: Trans-Assoc-Am-Physicians. 1979; 92292-302
AB: Dietary zinc intake was restricted (2.7-5.0 mg daily) for 24 to 40 weeks in five male volunteers. Their ages ranged from 51 to 65 years with a mean age of 57 years. Oligospermia was induced in all. In four subjects, oligospermia occurred 2 to 14 months after zinc restriction was instituted. In one subject, the onset of oligospermia was not accurately determined. The duration of oligospermia in the four subjects ranged from 6 to 14 months. Oligospermia was reversed after 2 to 32 months of zinc supplementation in physiologic amounts. The baseline sperm count (mean +/- SE) 289 +/- 85 millions/ml dropped to 33 +/- 4.5 millions/ml (P less than 0.05) following zinc restriction, and increased to 151 +/- 33 millions/ml after zinc supplementation (P less than 0.025). Oligospermia coincided with decline in Leydig cell function and was reversed in three subjects after zinc supplementation in low doses. Our study has demonstrated that dietary restriction of zinc can decrease sperm count, and that oligospermia induced by mild zinc deficiency is a reversible process. Oligospermia seems to be a sensitive indicator of zinc deficiency.
Record 109 of 109 in MEDLINE(R)+ (1975-1980)
TI: Maternal and fetal plasma zinc in pre-eclampsia.
AU: Bassiouni,-B-A; Foda,-A-I; Rafei,-A-A
SO: Eur-J-Obstet-Gynecol-Reprod-Biol. 1979 Apr; 9(2): 75-80
AB: Zinc is important for fetal growth and is involved in several important enzyme systems. Maternal and umbilical plasma zinc concentrations were determined in 52 parturient women with mild and severe pre-eclampsia, and were compared with those obtained from 20 women in labor whose pregnancies had progressed normally. A decrease in maternal as well as umbilical plasma zinc concentrations was observed in pre-eclamptic women, and this decrease was statistically significant in severe pre-eclampsia. The causes of these changes in plasma zinc concentrations in pre-eclampsia were discussed, and the possible adverse effects of zinc deficiency on the mother and fetus were mentioned. Low plasma zinc concentrations in pre-eclampsia may be a sign of zinc deficiency, implying possible risks to the mother and her fetus. It is recommended that maintenance of adequate dietary zinc nutrition during pregnancy, and particularly in pre-eclampsia, is important.