The role of reactive oxygen species in the pathogenesis of acute ethanol-induced gastric mucosal lesions and the effects of quercetin were evaluated in an experimental model. In addition, the effects of quercetin on gastric damage were evaluated histopathologically. Rats were divided into three groups as control rats, ethanol treated rats and ethanol+quercetin treated rats. Ethanol group was given a gastric gavage containing 1 ml of 80% ethanol (v/v) prepared in distilled water. Quercetin (200 mg/kg body wt.) was given by intragastric gavage 120 min before the administration of ethanol. Gastric tissue thiobarbituric acid reactive substance levels, carbonyl compounds, histamine levels and myeloperoxidase activities were found to be increased in ethanol treated rats and quercetin treatment reversed these increases. No statistically significant changes were found between all groups in catalase activity. The superoxide dismutase activity dropped significantly after ethanol treatment and quercetin treatment increased this enzyme activity. Gastric damage was confirmed histomorphometrically by significant increases in the number of mast cells and gastric erosions in ethanol treated rats. It was also confirmed that quercetin treatment significantly decreased the number of mast cells and reduced the area of gastric erosions. The results suggest that the gastroprotective effect of quercetin in this experimental model could be due to its antiperoxidative, antioxidant and antihistaminic effects.