Gastric hemorrhagic erosions were induced by the administration of platelet-activating factor (PAF). Gastric wall blood flow was decreased and thiobarbituric acid (TBA) reactants in the gastric mucosa were increased 10 min after PAF injection. SOD and catalase reduced gastric mucosal lesions and TBA reactants, but had no influence on gastric blood flow. In polymorphonuclear leukocytes (PMN)-depleted rats, gastric mucosal lesions and TBA reactants in the gastric mucosa were reduced and gastric blood flow were increased. PAF induced the superoxide production from rat PMN in a dose dependent manner. These results suggest that oxygen-derived free radicals produced by PMN and lipid peroxidation may play an important role in the pathogenesis of gastric mucosal injury induced by PAF.