MELATONIN PROTECTS AGAINST LEAD-INDUCED CARDIO TOXICITY: INVOLVEMENT OF ANTIOXIDANT MECHANISM

Objective: The objective of the present studies is to find out whether melatonin is capable of providing protection to rat heart against lead acetate induced oxidative damage. Methods: Rats of the first group were intraperitoneally (i.p.) injected with lead acetate [15mg/kg body weight(bw)], another group was pre-treated with melatonin (10 mg / kg, fed orally), the positive control group was fed melatonin (10 mg / kg bw), and the control animals received vehicle treatment i.p. for 7 consecutive days. Concentration of lead in cardiac tissue was estimated by AAS. The alterations in the activity of the different bio-marker enzymes of cardiac damage, levels of biomarkers of oxidative stress, activities of the antioxidant and some of the mitochondrial enzymes were studied. Histomorphological changes and alteration in tissue collagen level was also studied through H-E and Sirius red stainings respectively. Results: Treatment of rats with lead acetate at the indicated dose for seven consecutive days caused significant accumulation of lead in cardiac tissue , alterations of all the parameters studied and caused injury to the cardiac tissue. All these changes were ameliorated when the rats were pretreated with melatonin. Conclusion: The results of the current studies indicate melatonin’s ability to mitigate lead-induced oxidative damage in cardiac tissue of experimental rats possibly through its antioxidant mechanisms, and, may have future therapeutic relevance in humans exposed to lead environmentally or occupationally and in situations where chelation therapy has limited success.