Effect of leptin on peroxidation and antioxidant defense in ethanol-supplemented Mus musculus heart

The aim of the study was to evaluate the effect of exogenous mouse leptin on ethanol-induced cardiac toxicity in mice. Administering ethanol (6.32 g/kg body weight p.o.) to 4-week-old healthy mice for 45 days resulted in significantly elevated plasma levels of leptin, lactate dehydrogenase (LDH), cardiac lipid hydroperoxides (LOOH) and thiobarbituric acid reactive substances (TBARS) and significantly decreased cardiac superoxide dismutase, catalase, vitamin C, vitamin E, reduced glutathione and glutathione-dependent enzyme levels (glutathione peroxidase and glutathione S-transferase). Subsequent to the experimental induction of toxicity (i.e., after the initial period of 30 days) exogenous leptin was administered (230 microg/kg body weight i.p.) every alternate day for 15 days along with the daily dose of ethanol. Leptin administration to ethanol-treated mice significantly elevated the levels of plasma leptin, LDH and cardiac LOOH, TBARS, whereas the activity of antioxidant enzymes and the concentrations of vitamins C and E were further decreased significantly. These findings were consistent with our histological observations, confirming that leptin enhances cardiac toxicity in ethanol-supplemented mice.