RESUMO
Pregnant, pregnant and lactating and/or lactating groups of female rats were exposed to lead in the form of lead acetate in the drinking water at a dose level of 200 mg/L for periods of gestation only [GI], gestation and lactation [GII] and lactation only [GIII]. Blood samples, liver, brain and mammary gland were taken from the treated dams as well as brain tissue samples from their babies at the end of each exposure period. Lipid peroxidation and the activity of both reduced glutathione [GSH] and catalase enzymes were evaluated in liver and brain tissues of dams as well as in the brain tissue of babies. Determination of the residual level of lead was carried out in serum, liver and brain tissue of the dams. Histopathological examination was performed in the liver, brain and mammary gland tissues of treated dams. Our results revealed that exposure to lead induced oxidative tissue damage, which was reflected by significant increase in the level of malondialdehyde [MDA] and decreased activities of GSH and CAT in tissues of dams and babies. Residual concentrations of lead were significantly increased in brain, serum and liver in comparison to control group. The histopathological examination revealed marked histological alterations in the liver, brain and mammary gland of treated dams. This investigation indicated that the effect of lead was more obvious in gestation and lactation period [GII] than the other two periods [gestation only [GI] and lactation only [GIII]]. Also, it denoted that the brain is the primary target organ of lead poisoning