The impact of age on microsomal function, manifested by its ability to convert thyroid hormone thyroxine (T ) to triiodothyronine (T&), was investigated using four age '& ( ) -months). The data show impaired microsomal function with advancing age represented by a significant decrease in serum levels of T& and T&/T ratio. There was a decline in the liver glutathione (GSH), total proteins and serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and gamma- glutamyl transpeptidase (*GT). There was an-age associated increase in liver content of the lipid peroxidation products, thiobarituric acid (TBA)-reactants and the serum total protein.
++ , - . '(+ - / ' + -old) +0- 1-) mg/kg CdCl 2their controls were injected with distilled water. A higher susceptibility of senile rats to cadmium toxicity was manifested as a significantly higher decrease in their serum T& level and T&/T ratio than adult compared to control. A reduction in the adaptive response of senile animals was manifested by a less increase in hepatic GSH in senile than adult as compared to control. The level of hepatic TBA-reactants was significantly higher in treated than in control group. The increase was more pronounced in the senile group. A marked hepatic cellular damage indicated by an increase in the serum levels of the AST and ALT was more pronounced in senile compared with adult rats. Treatment resulted in a decrease in the serum *GT and liver triglycerides (TG). The decrease in both parameters was more evident in senile as compared to adult group.