Helicobacter pylori infection has been associated with stimulation of gastr
ic mucosal reactive oxygen species (ROS) production, and it was postulated
that ROS production is due to neutrophil infiltration and activation. The a
im of this study was to investigate the direct effect of H. pylori on ROS f
ormation in gastric epithelial cells in vitro. The human gastric cancer cel
l line HM02 was incubated with H., pylori for 24 hr, and the effects on cel
l number and the intracellular radical scavenger reduced glutathione (GSH)
were assessed. H. pylori caused a concentration-dependent reduction of cell
ular 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 Ii. pylori-in
duced decrease in cellular GSH concentrations. We conclude that H. pylori d
irectly decreases cellular GSH concentrations in gastric epithelial cells.
We suggest that this effect is caused by the release of ROS by H. pylori.