Abstract
Testosterone manifests some protective effects against benzene-induced toxicity in rats. However, mechanism of protection remains to be established. Data showed that testosterone modulates conjugation of reactive metabolites of benzene by influencing phase-II enzymes viz. glutathione-S-transferase, glutathione peroxidase, and catalase in both liver and kidney. These observations are supported by the opposite results obtained in castrated rats. It is postulated that testosterone decreases the formation of reactive oxygen species resulting into an increase in phase-II enzymes. Enhanced activity of these antioxidant enzymes is responsible for DNA strand repair as demonstrated by short comet tail length in liver and kidney of benzene and testosterone treated rats. Castration alters benzene pharmacokinetics by influencing these enzymes, a response which may be abolished by testosterone supplementation.
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