Helicobacter pylori substantially increases oxidative stress in indomethacin-exposed rat gastric mucosa.

Helicobacter pylori (H. pylori) often play an important role in the pathogenesis of gastritis, peptic ulcer, and probably also gastric cancer. Reactive oxygen species (ROS) produced by this bacterium may be one of the crucial factors whereby oxidative stress can play a role in the pathogenesis of ulcer disease. The aim of this study was to assess ROS activity and glutathione redox status, a principal cellular redox sensor, in H. pylori-associated indomethacin-induced gastric ulcers in rats. Gastric lesion was produced by intragastric administration of indomethacin (7 mg/kg) for three days followed by administration of H. pylori suspension (density 10(9) colony forming units). Animals receiving indomethacin only or followed by administration of H. pylori suspension were sacrificed after 11 and 18 days. ROS activity was assessed by the level of lipid peroxidation (LPO) and the glutathione redox status by the ratio between oxidized and reduced glutathione (GSSG/GSH). Indomethacin did not significantly increase the level of LPO and the GSSG/GSH ratio. When H. pylori suspension was given together with indomethacin the LPO was increased both on days 11 and 18 and GSSG/GSH on day 18. H. pylori, thus, substantially increases glutathione redox ratio and lipid peroxidation in gastric mucosa, which may play an important role in the pathological mechanisms of this bacterium. The findings support the idea that dietary antioxidants could be beneficial in combination therapy for eradication of H. pylori.