Effect of cadmium on glutathione metabolism and glucose 6-phosphate dehydrogenase in rat tissues : role of vitamin E and selenium

Cadmium induces oxidative stress in tissues by increasing lipid peroxidation (LPO) and by altering the antioxidant status in tissues. The antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), and other antioxidants such as vitamin E, ascorbic acid, glutathione (GSH), and selenium (Se), scavenge the free radicals and detoxify them. The changes in GSH metabolism and enzymes of HMP shunt may also be responsible for antioxidant function, as generation of NADPH is required for the activity of glutathione reductase (GSH-R) and GSH-Px. Rats were administered vitamin E, Se, or both, prior to Cd intoxication to find out whether pretreatment with these agents prevents Cd-induced oxidative changes. The GSH-R activity and GSH content in liver, kidney, and heart decreased due to Cd intoxication while animals administered vitamin E and Se, prior to Cd intoxication, showed in general no significant decrease in GSH-R activity and GSH content in tissues as compared to control. The glutathione-S-transferase (GST) activity in tissues increased due to Cd intoxication which diminished to near control levels in animals administered vitamin E and Se, prior to Cd intoxication. The glucose 6-phosphate dehydrogenase (G6PDH) activity decreased in liver and heart tissues upon Cd intoxication. The changes in G6PDH may alter NADPH generation, thus affecting GSH-R activity and GSH production. The results show that Cd-induced oxidative stress may be due to decreased GSH content in tissues which, in turn, may be due to diminished activity of GSH-R and NADPH generation, however, vitamin E and Se pretreatment to animals attenuate Cd-induced oxidative stress.