Protective effect of carnosine on adriamycin-induced oxidative heart damage in rats

Objective: Oxidative stress is one of the major factors involved in the pathogenesis of adriamycin (ADR)-induced cardiac dysfunction. The present study examined the antioxidant protective effects of carnosine (CAR) on adriamycin-induced cardiac damage in rats. Methods: Female Sprague Dawley rats were divided into four groups. Control (CONT, n=8, saline only i.v.); carnosine (CAR, n=8.10 mg/kg/day, i.v.); adriamycin (ADR, n=10.4 mg/kg four times every 2 days for 8 days, i.v.) alone and carnosine with adriamycin (CAR+ADR, n=10). Carnosine was given one week before adriamycin treatment and following one week with adriamycin treatment. After measurement of physiological func- tions, blood samples were collected for biochemical assays. The hearts were excised for hemodynamic study. Comparisons between different groups were made using ANOVA and posthoc Tukey test. Results: Adriamycin produced evident cardiac damage revealed by; hemodynamic changes - decreased left ventricular developed pressure (p 0.01), the maximum-minimum rates of change in left ventricular pressure (±dP/dt, p 0.01), electrocardiogram (ECG) changes (elevated ST, decreased R-wave, p 0.001), cardiac injury marker changes (increased creatine kinase, lactate dehydrogenase, aspartate aminotransferase and alanine aminotransferase), plasma antioxidant enzymes activity changes (decreased superoxide dismutase, glutathione peroxidase, catalase activities, p 0.03) and lipid peroxidation (elevated malondialdehyde, p 0.05) to the control and carnosine groups. Carnosine treatment caused significant attenuation (p 0.05) of cardiac dysfunction induced by adriamycin (CAR+ADR), revealed by normalization of the ventricular function, ECG and biochemical variables. Conclusion: An increase in oxidative stress, superoxide dismutase, glutathione peroxidase levels, catalase inactivation and cardiac dysfunction induced by adriamycin were prevented by carnosine.