PRODUCTS OF NEUTROPHIL METABOLISM INCREASE AMMONIA-INDUCED GASTRIC-MUCOSAL DAMAGE

Recent studies have indicated that ammonia is involved in the pathioph ysiology of Helicobacter pylori-associated gastric mucosal damage. Hel icobacter pylori-associated chronic active gastritis is characterized by an invasion of neutrophils. We investigated the interrelationship a mong hypochlorous acid (oxidant produced by neutrophil), ammonia (prod uct of Helicobacter pylori urease), and monochloramine (product of amm onia and hypochlorous acid) in the development of gastric mucosal dama ge in rats. Gastric mucosal lesions were produced by exposure of the g astric mucosa to ammonia, urea with urease, or urea with Helicobacter pylori in rats subjected to ischemia. Pretreatment with taurine (scave nger of hypochlorous acid) or antineutrophil serum significantly atten uated gastric mucosal lesions induced by the above test agents. Ammoni a-induced gastric mucosal lesions were exacerbated in the presence of hypochlorous acid with concomitant generation of monochloramine. These results suggest that the ammonia, hypochlorous acid, and monochlorami ne triad may be important in Helicobacter pylori-mediated gastric muco sal damage.