The interrelationships between the development of ethanol-, HCl, NaOH and NaCl-induced gastric mucosal damage and the gastric mucosal superoxide dismutase activity in the rats.

Gastric mucosal damage was produced by intragastric administration of 96% ethanol, 0.6 M HCl, 0.2 M NaOH or 25% NaCl. The animals were killed 1 hr later, when the number and severity of gastric lesions (ulcers) was recorded. At the time of the sacrifice of the animals gastric mucosal superoxide dismutase (SOD) activity was measured. It was found that (1) the gastric mucosal damage could be induced by the administration of any of the necrotizing agents in all animals, (2) superoxide dismutase (SOD) activity increased significantly in the damaged gastric mucosa following 96% ethanol, while its activity decreased significantly during the development of gastric mucosal damage produced by the intragastric administration of 0.6 M HCl, 0.2 M NaOH or 25% NaCl. It has been concluded that: (1) the enzyme systems necessary to generate the superoxide free radical anions can be stimulated by ethanol, and they can be inhibited by the application of 0.6 M HCl, 0.2 M NaOH and 25% NaCl: (2) the observed stimulation or inhibition of the enzyme systems to generate the superoxide free radical anions may be of pathological significance in the development of gastric mucosal damage produced by the intragastric administration of 96% ethanol, 0.6 M HCl, 0.2 M. NaOH or 25% NaCl.