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An investigation of the influence of dietary zinc (8, 35, 200 ppm) on the toxicity of dietary lead (0, 50, 200 ppm) in the young male rat in a seven week period indicated that as dietary zinc increased, the severity of lead toxicity decreased. Evidence included decreased lead concentration in blood, liver, kidneys, and tibias; decreased excretion of urinary delta-aminolevulinic acid; decreased accumulation of free erythrocyte porphyrins; decreased inhibition of kidney delta-aminolevulinic acid dehydrase activity; and a decrease in apparent lead absorption. Infected zinc did not afford protection against lead toxicity. The data indicate that the protective effect of zinc on lead toxicity is largely mediated by an inhibition of lead absorption at the intestinal level.

The influence of ascorbic acid supplementation on the copper status of young adult men was investigated. Subjects consuming self-selected diets took 500 mg of ascorbic acid with each meal (1500 mg/day) for 64 days. Blood samples were obtained at 0, 28, 52, and 64 days in order to determine serum copper and serum ceruloplasmin. Each subject thus served as his own control. Analyses were repeated 20 days after the ascorbic acid supplement was terminated. Serum ceruloplasmin activity was significantly reduced (p less than 0.01) at every data point throughout the ascorbic acid supplementation period. A similar but nonsignificant trend was observed for serum copper. Furthermore there was a significant increase (p less than 0.01) in serum copper concentration 20 days after the supplementation period. Although observed effects occurred within physiological ranges of normal values, this study confirms that a high ascorbic acid intake is antagonistic to copper status of men as has been demonstrated in laboratory animals.

An investigation of the influence of dietary selenium (0.015, 0.05, 0.50, 1.0 ppm) on toxicity of dietary lead (0 and 200 ppm) in the young male rat indicated that selenium was mildly protective against the toxic effects of lead, but only up to 0.50 ppm selenium. At the excess selenium dietary level an exaggeration of lead toxicity was observed. Criteria employed to judge the effects of dietary selenium on lead toxicity included tissue lead concentration and urinary delta-aminolevulinic acid excretion. One exception to the exaggeration effect of excess selenium on lead toxicity was the protective effect of selenium on liver delta-aminolevulinic acid dehydratase activity. Since lead depressed kidney selenium concentration, lead may act as an antagonist to selenium metabolism.

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