Reactive oxygen species activity, mucosal lipoperoxidation and glutathione in Helicobacter pylori-infected gastric mucosa

Background and Aim: Helicobacter pylori is considered as the major pathogen in Helicobacter pylori-associated gastroduodenal disease, but the mechanism of its action has not been fully explained. This study was performed to assess the reactive oxygen species activity and the damage in Helicobacter pylori-infected gastric mucosa. Methods: Gastric biopsy specimens were obtained from 308 patients undergoing endoscopy. Gastric mucosal damage was assessed by using luminol enhanced chemiluminescence, thiobarbituric acid-reactive substance, and mucosal glutathione. Results: The chemiluminescence and thiobarbituric acid-reactive substance-equivalent levels in the mucosa of patients with Helicobacter pylori-positive gastric mucosa (43.8 ± 134.9 c.p.m./μg tissue, 157.0 ± 96.2 nmol/g tissue, respectively) were significantly higher than in those with Helicobacter pylori-negative mucosa (6.8 ± 20.3 c.p.m./μg tissue, 110.0 ± 51.6 nmol/g tissue, respectively; P = 0.000, P = 0.016, respectively). The glutathione levels in the mucosa of patients with Helicobacter pylori-positive gastric mucosa (159.3 ± 76.6 nmol/μg tissue) were significantly lower than in those with Helicobacter pylori-negative gastric mucosa (212.3 ± 134.3 nmol/μg tissue; P = 0.008). After the data were divided according to the presence of Helicobacter pylori, there were no significant differences in chemiluminescence, thiobarbituric acid-reactive substance, and glutathione among the different macroscopic findings within Helicobacter pylori-positive and -negative gastric mucosa. Conclusions: Helicobacter pylori infection plays a pathological role in many gastrointestinal diseases through excessive mucosal-reactive oxygen species production, pronounced membrane damage, and the depletion of gastric anti-oxidants.