Role of lipid peroxidation and polymorphonuclear leukocytes-derived oxygen radicals in acute gastric lesions induced by hyperthermic treatment.

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Acute gastric lesions were experimentally induced by local hyperthermic treatment (42°C, 40 min). Thiobarbituric acid (TBA) reactants in the gastric mucosa were significantly increased 40 min after the hyperthermia. There were no changes in gastric mucosal blood flow and gastric acid secretion. The total area of gastric erosions and TBA reactant in gastric mucosa of rats deficient in vitamin E were significantly increased compared with those of rats supplemented with vitamin E. The increase in the total area of gastric erosions and TBA reactants in gastric mucosa were significantly inhibited by the treatment of bovine Cu, Zn-SOD and bovine catalase, and by the depletion of polymorphonuclear leukocytes (PMN). Allopurinol did not show any influence on these pathological changes induced by hyperthermia. These results suggest that lipid peroxidation and PMN-derived oxygen radicals may play an important role in the pathogenesis of gastric lesions induced by hyperthermic treatment.