The effects of acute or chronic lead (7439921) administration on urinary zinc excretion were investigated in rats. In acute experiments, male Charles-River-rats were intravenously administered acetate in dextrose. Urine was then collected for the next 6 hours. In chronic experiments, following 6 day baseline urine collections, male rats received either sodium-acetate or 500 parts per million (ppm) lead-acetate in demineralized drinking water, free choice, for 12 days. As water intake was self restricted in lead exposed animals, drinking water was matched in both groups in the following 50 days. On experimental day 43, both groups were switched from a diet with 20ppm zinc to a low zinc diet with 80 to 10ppm zinc. Throughout the experiment urine and plasma zinc concentrations, plasma sodium, potassium, zinc, creatinine, and renin activity were measured. One testis and one kidney were taken from each rat for zinc analysis. Acute lead exposure of 0.03 or 0.3mg/kg did not alter urinary zinc excretion, but excretion was significantly elevated in animals receiving 3mg/kg lead. Urine volume, sodium or potassium excretion, plasma zinc concentrations, and body weights showed no significant differences between any groups. In chronic testing, zinc excretion in lead treated animals began consistently to exceed that of controls by day 2, continuing through day 35, partly due to an unexplained decrease in control zinc excretion. By day 17, control zinc excretion returned to baseline, but zinc excretion in lead treated rats continued to exceed control values through day 34, being approximately 2 fold. Urinary zinc excretion was unaffected by water restriction, but from day 36 on, there were no consistent differences in zinc excretion between groups. Only testis weight and zinc content were significantly decreased in lead exposed animals, while plasma renin activity was 2 fold in this group. The authors conclude that acute or chronic lead exposure causes increased urinary zinc excretion.