Effect of copper-hydroquinone complex on oxidative stress-related parameters in human erythrocytes (in vitro)

The effect of in vitro exposure of human erythrocytes to micromolar concentrations of hydroquinone and copper simultaneously on oxidative status-related biochemical parameters was studied. Hydroquinone is a component of cigarette smoke and serum copper level is increased in smokers. Copper forms a complex with hydroquinone and enhances its auto-oxidation to benzoquinone which covalently binds to sulfhydryl group containing compounds like reduced glutathione. In this study, copper increased H(2)O(2) production by hydroquinone. Hydroquinone either alone or in the presence of copper produced a decrease of reduced glutathione level without altering methemoglobin concentration and erythrocyte lipid peroxidation. Catalase inhibition by sodium azide depleted reduced glutathione level further. Copper-hydroquinone complex mediated glutathione depletion in the catalase containing RBC was not decreased by antioxidant, butylated hydroxytoluene. From the known facts and above findings, it is suggested that depletion of reduced glutathione by hydroquinone in the presence of copper in catalase active RBC may be due to the formation of 1, 4 benzoquinone adduct of reduced glutathione and to some extent due to binding of copper to the thiol group of reduced glutathione rather than conversion to oxidized glutathione via reactive oxygen species. Depletion of reduced glutathione by N-ethylmaleimide pretreatment followed by copper-hydroquinone treatment had no effect on methemoglobin level or lipid peroxidation. Furthermore, copper-hydroquinone complex did not increase erythrocyte susceptibility to oxidative stress. This suggests hydroquinone in the presence of copper does not contribute to erythrocyte membrane lipid peroxidation seen in smokers. Criteria for ideal antioxidant supplementation in smokers were suggested.