• A A Mylroie, H Collins, C Umbles, and J Kyle.
• Toxicol. Appl. Pharmacol. 1986 Mar 15; 82 (3): 512-20.

AbstractThe effects of lead ingestion on parameters indicative of copper status, and particularly on the activity of the copper-dependent metalloenzyme superoxide dismutase (SOD) in erythrocytes, were investigated in weanling and neonatal rats. In a series of experiments, Sprague-Dawley or Long-Evans rats were fed a nutritionally adequate purified diet (AIN-'76). Lead acetate was given orally in the drinking water (0, 100, 250, or 500 ppm Pb) to groups of 23 to 26-day-old rats for 5 weeks or intragastrically (0, 5, 11, 22, or 45 mg Pb/kg body wt/day) to pups from postnatal Days 2 through 20. Lead ingestion (250 and 500 ppm Pb) by weanling rats resulted in decreased concentrations of copper in blood (erythrocytes and serum), liver, and spleen, in increased concentrations of iron in liver and spleen, in increased spleen weight, and in a small decrease in hemoglobin and hematocrit values. There was a significant decrease in the activities of the copper metalloproteins erythrocyte superoxide dismutase (SOD) and serum ceruloplasmin (Cp). In contrast, in the neonate we found no significant effects of lead on copper concentrations in blood or tissue or on other measures indicative of copper status. Despite high blood lead concentrations (1-3 micrograms/ml), SOD activity was not decreased in the neonatal rat. In addition, lead had no direct effect in vitro on the activity of bovine blood superoxide dismutase. On the basis of both the in vitro and in vivo studies, it appears likely that the observed decrease in SOD in young rats is caused indirectly by a lead-induced copper deficiency rather than by a direct inhibitory effect of lead.

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