Relationship between oxidative stress and heme oxygenase induction by copper sulfate”.

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

ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS

Año: 1997 vol. 337 p. 332 - 337

0003-9861

The effect of copper sulfate (CuSO4) on both hepatic oxidative stress and heme oxygenase induction was studied. A strong increase inin vivorat liver chemiluminescence was observed 1 h after Cu(II) administration. To evaluate liver antioxidant enzymatic defenses, superoxide dismutase, catalase, and glutathione peroxidase activities were determined. Catalase and glutathione peroxidase were found to be significantly decreased 5 h after CuSO4injection. In contrast, superoxide dismutase activity was increased. Heme oxygenase activity appeared 5 h after treatment, reaching a maximum value 18 h after CuSO4administration. This induction was preceded by a decrease in the intrahepatic GSH pool and an increase in the generation of thiobarbituric acid reactive substances, both effects taking place a number of hours before induction of heme oxygenase. Administration of bilirubin, 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 chemiluminescence when administered 2 h before CuSO4treatment. 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 induction and oxidative stress.