This study was carried out to evaluate whether the pyridoindole stobadine (STO), which is an effective cardioprotective drug and a potent antioxidant, had any specific role in changes Of lysosomal enzyme (LE) activity in the rat heart during oxidative stress induced by a high dose of a synthetic catecholamine, isoproterenol (IPN). Oxidative stress induced by catecholamines is a well recognized toxic event. This effect has been extensively observed in the heart, where high levels of catecholamines cause lipid peroxidation, energy depletion and myocardial necrosis accompanied with leakage of lysosomal content and subsequent LE activity changes in most mammals. The activities of the LE acid phosphatase and N-acetyl-ß-D-glucosaminidase were studied in the rat heart as markers of cell damage. IPN-induced toxic damage in male Wistar rats (9 h after IPN hydrochloride administration, 50 mg/kg s.c. ) was manifested by marked alterations in the activities of the LE in the sedimentable fraction of the rat myocardium. STO administered in various dosage regimens reduced or diminished the IPN-induced biochemical changes in the rat myocardium. The results suggest that STO is able to protect rats against IPN-induced oxidative stress.

Keywords: Toxicology; stobadine; oxidative stress