Inhibitory effect of melatonin on products of lipid peroxidation resultingfrom chronic ethanol administration

Despite decades of research, the role of free radicals in alcohol-induced o rgan injury is still a matter of debate. The present work was designed to i nvestigate the potential protective effect of melatonin, a reported radical scavenger and antioxidant, on free radical toxicity induced by chronic eth anol administration. The major end-point of oxidative damage measured in th is report was lipid peroxidation. Four groups of male Sprague-Dawley rats w ere used. The first group served as untreated controls and received a daily injection of alcoholic (<1% ethanol) saline. The second group of rats rece ived daily at 18:00 a single subcutaneous injection of melatonin (10 mg/kg) . Group a rats received only ethanol (3 g/kg) for 30 consecutive days; the ethanol was given at 18:30. The final group of rats was given both melatoni n and ethanol with melatonin preceding ethanol by 30 min. Products of lipid peroxidation [malondialdehyde (MDA) and 4-hydroxyalkenals (4-HDA)] were me asured in the brain, heart, liver lung and testes. At the conclusion of the study, MDA + 4-HDA levels were significantly increased in brains, hearts, lungs and testes, but not livers, of alcohol-treated compared with control rats. The percentage increases in lipid peroxidation products were 21.8%, 2 8.8%, 35.9% and 45.3% for brain, heart, lung and testes. respectively. In a nimals given melatonin 30 min before ethanol, the increases in MDA + 4-HDA levels were significantly reduced in all organs investigated, with levels n ot different from those in control mts. Based on these findings, it is spec ulated that melatonin's direct and indirect antioxidative actions inhibited alcohol-induced lipid peroxidation. These results suggest a new strategy f or the treatment of alcohol-related diseases using melatonin as an antioxid ant to reduce the damage inflicted by aggressive radical species.