Helicobacter pylori reduces intracellular glutathione in gastric epithelial cells.

Helicobacter pylori infection has been associated with stimulation of gastric mucosal reactive oxygen species (ROS) production, and it was postulated that ROS production is due to neutrophil infiltration and activation. The aim of this study was to investigate the direct effect of H. pylori on ROS formation in gastric epithelial cells in vitro. The human gastric cancer cell line HM02 was incubated with H. pylori for 24 hr, and the effects on cell number and the intracellular radical scavenger reduced glutathione (GSH) were assessed. H. pylori caused a concentration-dependent reduction of cellular GSH concentrations over a broad bacteria-to-cell ratio (1.4-42) in the absence of cell necrosis. The radical scavengers MnTBAP (a cell permeable superoxide dismutase) and ebselen provided protection against H. pylori-induced decrease in cellular GSH concentrations. We conclude that H. pylori directly decreases cellular GSH concentrations in gastric epithelial cells. We suggest that this effect is caused by the release of ROS by H. pylori.