Role of Catalase in Ischemia-Reperfusion Injury in the Perfused Rat Heart

Endogenous hydrogen peroxide (H2O2), which is generated invariably in normal cells, serves as a precursor for highly reactive oxygen intermediates. Although cellular function is equipped with an effective defense mechanism against the action of H2O2, the activity of the defense mechanism has been reported to decrease during Ischemia-reperfusion. Though H2O2 is cataiytically reduced to H2O by either catalase or glutathione peroxidase, the amount of catalase activity in the heart tissue is much lower than in another organs and its role is still uncertain. In the present study we investigated the role of catalase as a defense mechanism against reperfusion injury. Catalase was inhibited by intraperitoneal injection of 3-amino-1, 2, 4-triazole (ATZ) 30 min before the excision of the rat heart. After 20 min of reperfusion following 10 min of global Ischemia, the sarcoplasmic reticulum (SR) was extracted by centrifuga-tion. We found that ATZ treatment significantly affected recovery of the contractile function during reperfusion. Ca2+-ATPase activity and the content of the major ATPase protein of the SR after reperfusion were significantly decreased by ATZ, indicating degradation of the SR. The results indicate that catalase is an important cellular defense mechanism that alleviates the toxic effect of endogenous H2O2 in the myocardium during ischemia-reperfusion.