RESUMO
Chronic ethanol administration has been found to have neuronal damaging effect through free radical generation. The aim of this study is to determine the possible neuroprotective effect of melatonin [MLT] against ethanol induced neuronal damage in the brain stem of male albino rats. Rats were randomly divided into 3 groups: control group, 35% ethanol-treated group and melatonin [l0mg/kg I. P. for 7 consecutive days] pre-treated ethanol group. Administration of ethanol [35%] orally in drinking water for 30 consecutive days decreased glutathione [GSH], dopamine [DA], norepinephrine [NE] and serotonin [5-HT] contents and superoxide dismutase [SOD] activity. The maximal percentage of decrease was 44%, 34%, 41%, 29% and 40%, respectively. On the other hand; there was a progressive increase in malondialdehyde [MDA] level and DNA fragmentation by 128% and 53%, respectively. Melatonin administration prior to ethanol significantly increased. GSH, DA, 5-HT, and NE contents in brain stem by 53%, 30%, 33%, 33% respectively and SOD activity by 35%. MDA level and DNA fragmentation were markedly reduced by 36% and 30%, respectively. Our data suggest that melatonin is capable of at least partially preventing ethanol -induced neurodegeneration in the brain stem of rats. This effect might be attributed to direct free radical scavenging properties and regulation of antioxidative enzyme activity of melatonin