Lipid peroxidation and anti-oxidant defence in human gastric mucosa: Effect of Helicobacter pylori

Aim: The mechanisms underlying chronic gastric damage and the correlation between Helicobacter pylori infection and gastric carcinogenesis are poorly understood. We therefore planned a study to show whether H. pylori infection is related to increased free radical production and lipid peroxidation in the stomach and whether anti-oxidant defences are altered. Design: We measured gastric mucosal reduced and oxidized glutathione, and malondialdehyde, as an indication of lipid peroxidation in 107 patients undergoing upper gastrointestinal tract endoscopy. Results: The reduced-glutathione levels were not significantly modified by the presence of either chronic gastritis or chronic atrophic gastritis, nor by the presence of H. pylori infection, even though a trend towards increased levels was observed in both instances. Oxidized glutathione was significantly affected by the presence of gastric damage (P < 0.05). Malondialdehyde levels were significantly higher in patients with chronic atrophic gastritis (P = 0.029) and in the presence of H. pylori infection (P = 0.03). When the patients were grouped according to disease activity, both H. pylori infection (P = 0.0001) and malondialdehyde levels (P = 0.01) were significantly associated with higher activity. Conclusions: Free radical production and lipid peroxidation in the gastric mucosa depend on the presence and extent of gastric damage and, independently, on the presence of H. pylori infection