HELICOBACTER-PYLORI, FREE-RADICALS AND GASTRODUODENAL DISEASE

Free radicals, or reactive oxygen metabolites, are products of normal metabolism, but can cause human disease when produced in excess. Mucosal pathology related to Helicobacter pylori infection, in both the stomach and duodenum, could be explained by locally acting toxic factors such as cytotoxin, urease and ammonia: the possibility that reactive oxygen metabolites could act like such toxic factors has received tittle attention. However, there is now a growing body of evidence that H. pylori causes mucosal damage partly through attraction followed by activation of phagocytes, producing excessive reactive oxygen metabolites. Direct and indirect evidence of reactive oxygen metabolite excess in association with human duodenal ulceration and H. pylori-related gastritis, stimulation of reactive oxygen metabolite production from phagocytes by H. pylori and its soluble products in vitro, and healing of duodenal ulceration using anti-oxidants have all been reported over the last 3 years. This paper reviews this evidence, the mechanisms by which reactive oxygen metabolites might produce gastroduodenal mucosal injury, their potential links with gastric carcinogenesis and implications for treatment.