Abstract
Cardiac metabolism of H2O2 was studied by determining the concentration dependence for H2O2-stimulated release of GSSG, an indicator for flux through the glutathione peroxidase pathway, in perfused heart preparations. Treatment of rats with aminotriazole in vivo inhibited heart catalase by 83% and shifted the doseresponse curve for GSSG release toward lower H2O2 concentrations. In aminotriazole-treated rats, 50 μM H2O2 elicited a maximal rate of GSSG release (about 5 nmol per g heart), whereas 200 μM H2O2 was necessary for obtaining a similar rate of GSSG release in control rat hearts. The results show that catalase, although present at low levels of activity in the heart compared to other organs, functions as a major route for detoxication of H2O2 in the myocardium.