Abstract
Repeated administration of a small dose of compound 48/80 induced acute gastric mucosal injury in rats. Thiobarbituric acid (TBA) reactants in the gastric mucosa were significantly increased and serum alpha-tocopherol was significantly decreased after the treatment. The total area of gastric lesions and the increase in TBA reactants in the gastric mucosa were significantly reduced by pretreatment with superoxide dismutase (SOD) and/or catalase, allopurinol and anti-rat polymorphonuclear leukocytes (PMN) antibody. Lipid peroxidation and oxygen radicals derived from both the xanthine-xanthine oxidase system and PMN may be involved in the pathogenesis of compound 48/80-induced gastric mucosal injury.
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