AMMONIA PRODUCED BY HELICOBACTER-PYLORI, RELATED TO SUPEROXIDE GENERATION IN-SITU, AS A MAJOR FACTOR IN ACUTE GASTRITIS

Purpose: To evaluate (1) the effects of Helicobacter pylori on inflamm ation of gastric mucosa in animal models by histopathological examinat ion and by assessing the generation of active oxidants in situ; and (2 ) the relationship between the infiltration of polymorphonuclear cells in the gastric mucosa and active oxidants stimulated by H. pylori. St udy selection: Animal models such as rabbits and Japanese macaques wer e used for microscopic examinations and for measurements of chemilumin escence, using a Cypridina luciferin analog, phenyl-3,7-dihydroimidazo [1,2-alpha]pyrazin-3-one, as a chemiluminescence probe that responded to the generation of superoxides and singlet oxygen radicals. Results: In rabbits, increased chemiluminescence intensity was measured in gas tric mucosa after the administration of 294 mmol/l (0.5%) ammonia or a mixture of H. pylori and 83 mmol/l (0.5%) urea solution, and was inhi bited by the administration of superoxide dismutase. Histopathological examinations showed acute inflammations in both treatment groups; in particular, polymorphonuclear cells had infiltrated into gastric mucos a. In Japanese macaques inoculated with H. pylori, a similar infiltrat ion of polymorphonuclear cells into gastric mucosa was observed, and a decreased chemiluminescence intensity was observed during administrat ion of superoxide dismutase 24 h after the treatment. Conclusions: Amm onia produced by H. pylori is a major factor in the acute inflammation related to superoxide generation from gastric mucosa in situ.