State of pregnancy modifies lead toxicity in mice.

Toxicity of lead acetate after administration through the oral route at 0-50 mg/kg body weight of animal has been assessed in the liver of pregnant mice and compared with the effect in the liver of nonpregnant dams. Analysis showed that the basal level of hepatic lead is considerably reduced during pregnancy as compared to that in nonpregnant state. After administration of Pb-acetate, deposited lead in liver of nonpregnant mice was 3- to 4-fold while in pregnant mice was, it was 1.8- to 3.0-fold over their respective control values. Although hepatic Fe, Cu, and Zn levels had a tendency to be lowered during pregnancy, it appeared that the added trace quantity of lead prior to and during pregnancy helped in the retention of these metals, which either remained unaffected (as Fe) or declined (Cu and Zn) after lead administration during the nonpregnant state. The effect of lead on Mn diminution, however, was visible at the dose of 50 mg/kg body wt of lead-acetate. Alkaline phosphatase, which increased during pregnancy along with Mn, was reversed between the pregnant and nonpregnant states after oral administration of lead. On the other hand, the level of delta-aminolevolunic acid dehydratase, which declined during normal pregnancy, continued to fall further after lead exposure. It is concluded that the distribution of basal or administered lead and its effect on enzyme activities and trace metal composition in liver depends on the pregnant and nonpregnant states of female hosts.