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.
Lipid peroxidation and anti-oxidant defence in human gastric mucosa: Effect of Helicobacter pylori / Farinati, F.; Cardin, R.; Della Libera, G.; Rugge, M.; Di Mario, F.. - In: EUROPEAN JOURNAL OF GASTROENTEROLOGY & HEPATOLOGY. - ISSN 0954-691X. - 5:SUPPL. 2(1993), p. -S11.
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