Abstract
In platelet activating factor (PAF) or compound 48/80 (C48/80)-induced gastric injury in rats, gastric mucosal blood flow was decreased and thiobarbituric acid (TBA) reactants in the gastric mucosa were increased. Gastric injury and the increase in TBA reactants in the gastric mucosa were inhibited in rats treated with superoxide dismutase (SOD) and/or catalase, and in polymorphonuclear leukocyte (PMN)-depleted rats. Oxygen radicals derived from PMN and lipid peroxidation may be involved in the pathogenesis of gastric injury in these models.
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