The role of zinc in gonadal function was investigated in rats. The increases in luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone were assayed after intravenous administration of synthetic luteinizing-hormone-releasing hormone (LHRH) to zinc-deficient and restricted-fed control rats. Body weight gain, zinc content of testes, and weight of testes were significantly lower in the zinc-deficient rats compared with the controls. The serum LH and FSH response to LHRH administration were higher in the zinc-deficient rats but serum testosterone response was lower in comparison with the restricted-fed controls. These studies indicate a specific effect of zinc on testes and suggest that gonadal function in zinc-deficient state is affected through some alteration of testicular steroidogenesis.

The epidemiological aspects of oral contraceptive agents on nutrient metabolism were studied in a large population of women. Incidence of clinical abnormalities, related to malnutrition, were more frequently observed in the lower (B) as compared to the higher (A) socioeconomic groups. In the A groups some clinical signs were more common in the nonsupplemented groups of subjects. In general, the intake of oral contraceptive agent subjects for calories, protein, calcium, magnesium, iron, copper and zinc did not differ from the controls. The intake of the above nutrients in group A subjects were higher than those of group B except for calories. The subjects who took supplements had higher intakes of calcium, iron, magnesium and copper. No effect of oral contraceptive agents was seen on hemoglobin, hematocrit and erythrocyte count. Serum iron was increased due to "Norinyl." Total iron binding capacity was increased as a result of oral contraceptive agent administration. Total iron binding capacity values were higher in group B as compared to group A and in the nonsupplemented as compared to the supplemented groups. Plasma copper was increased and plasma zinc was decreased as a result of oral contraceptive agent administration. An increase in erythrocyte zinc was observed due to "Norinyl." No effect of oral contraceptive agents on plasma calcium, magnesium and erythrocyte magnesium was observed. Although no effect of oral contraceptive agents on plasma total protein was found, serum albumin was decreased.

Clinical, biochemical and nutritional data were collected from a large population of women using oral contraceptive agents. Higher incidence of abnormal clinical signs related to malnutrition were observed in the lower (B) as compared to the higher (A) socioeconomic groups, and also in the nonsupplemented groups as compared to the supplemented groups in the B subjects. As a rule the intake of oral contraceptive agent subjects of vitamin A, C, B6 and folic acid did not differ from that of the controls As expected, subjects from the supplemented groups had higher intake of vitamin A, C, B6, thiamin, riboflavin and folic acid, and A groups had higher intake of vitamin C, B6, riboflavin and folic acid. Increased plasma vitamin A and decreased carotene levels were observed in oral contraceptive agent users. In general oral contraceptive agents had little or no effect on plasma ascorbic acid. Urinary excretion of both thiamin and riboflavin in subjects using oral contraceptive agents were lower in A groups. Erythrocyte folate and plasma pyridoxal phosphate was decreased in A groups due to oral contraceptive agents. Subjects who took supplements had higher levels of plasma vitamin A, ascorbic acid and folate. But urinary thiamin and riboflavin were higher only in group A subjects who took supplements.

The effects of graded levels of dietary zinc on the development and mineralization of teeth and bones and on the susceptibility of teeth to dental caries were studied in young growing rats. Thirty-six weanling male Sprague-Dawley rats were randomly assigned to four dietary treatments: 1) zinc-deficient, less than 1 ppm; 2) 12 ppm zinc; 3) 36 ppm zinc, and 4) 108 ppm zinc. For treatments 2, 3 and 4, rats were pair-fed the quantity of feed consumed by their individual counterparts fed the zinc-deficient diet. After 4 weeks of treatment, growth retardation along with other clinical zinc deficiency signs were observed in rats fed the zinc-deficient diet. The zinc levels in bones and teeth of zinc-deficient rats were lower than those for rats fed supplemental zinc. Increased dietary zinc resulted in greater levels of zinc in bones and teeth, but the levels of calcium decreased. Greater incidences of enamel lesions in mandibular molars were observed in rats fed the zinc-deficient diet than in rats pair-fed zinc-supplemented diets. Furthermore, the effect of zinc deficiency on dental caries of young rats was predominantly at the smooth surfaces of the molars. Dietary zinc may be an important trace mineral in the process of post-eruptive mineralization of the enamel and may reduce the susceptibility of teeth to caries.

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