Abstract

Cadmium (Cd; 10–100 μM) produced in isolated hepatocytes the formation of thiobarbituric acid-reactants (lipid peroxidation; LPO) and a decrease in SH groups in a time- and concentration-dependent manner. However, glutathione peroxidase (GSH-Px) was not affected indicating that LPO does not originate from GSH-Px injury. In contrast, in presence of Cd a time- and concentration-dependent decrease of glucose-6-phosphate dehydrogenase (G6PDH) and, most strongly, of glutathione reductase (GSSG-R), both members of the GSH-Px system, was observed. These effects could not be inhibited by ( + )-cyanidanol-3, a compound known as inhibitor of LPO. Therefore, our data show that (l)Cd-induced LPO is not a function of GSH-Px injury and (2) inhibition of GSSG-R and G6PDH-activity is not a function of LPO. They also indicate that Cd-induced depletion of cellular SH groups are associated with toxic effects of Cd on GSSG-R and G6PDH different from LPO-induction.

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