Melatonin prevents ethanol-induced gastric mucosal damage possibly due to its antioxidant effect

Oxygen radical release has been proposed as a pathogenic factor of the ethanol-induced acute gastric injury. Melatonin, a pineal hormone, is known to scavenge oxygen free radicals. We investigated whether parenteral administration of melatonin prevented ethanol-induced macroscopic damage, polymorphonuclear (PMN) leukocyte infiltration, depletion of total glutathione (tGSH) concentration, and glutathione reductase (GSSG-Rd) activity in the rat gastric mucosa. We compared the effects of melatonin with those of omeprazole. Ethanol-induced mucosal damage was evaluated using three different parameters: gastric total glutathione (tGSH) concentration and glutathione reductase (GSSG-Rd) activity, the number of PMN leukocytes, and macroscopic investigation. Gatric tGSH concentration and GSSG-Rd activity decreased and the number of PMNs increased after ethanol administration. It was found that pretreatment with melatonin increased both tGSH concentration and GSSG-Rd activity. Melatonin also reduced ethanol-induced PMN infiltration in the stomach. Ethanol administration damaged the entire gastric mucosa. Melatonin significantly decreased the extent of ethanol-induced macroscopic injury. In conclusion, these findings support the conclusion that the protection conferred by melatonin in gastric ulcer is presumably due to its antioxidant activity.