Relationship between oxidative stress and heme oxygenase induction by copper sulfate

J.O. OSSOLA; M.D. GROPPA; M.L. TOMARO

Pucón. Chile

Congreso; VIII Congreso de la Pan-American Association for Biochemistry and Molecular Biology (PABMP).; 1996

Asociación Panamericana de Sociedades de Bioquímica y Biología Molecular

The effect of copper sulfate on both, hepatic oxidative stress and heme oxygenase (HO) induction was studied. A strong increase in “in vivo” rat liver chemiluminescence (QLV) was observed 1h after Cu(II) administration. To evaluate liver antioxidant enzymatic defenses, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-px) activities were determined. CAT and GSH-px were found to be significantly declined 5 h after Cu(II) injection. On the contrary, SOD activity was increased. HO activity appeared 5 h after treatment, reaching a maximum value 18 h after Cu(II) administration. This induction was preceded by a decrease in the intrahepatic GSH pool and an increase in the generation of thiobarbituric acid reactive substances (TBARS), both effects taking place some hours before induction of the heme oxygenase. Administration of bilirrubin, the end product of heme catabolism in mammals, and α-tocopherol, a widely employed antioxidant, completely prevented heme oxygenase induction as well as the decrease in hepatic GSH and the increase in QLV when administered 2 h before copper sulfate treatment. Under the same experimental conditions, β-carotene showed a moderate preventive effect on both, heme oxygenase induction and oxidative stress parameters. These data obtained with Cu(II) treatment are in agreement with our previous reports suggesting a correlation between heme oxygenase and oxidative stress.