Helicobacter pylori causes DNA damage in gastric epithelial cells

Helicobacter pylori infection has been considered as a risk factor for gast ric carcinoma. Strong evidence exists that reactive oxygen species (ROS) pl ay an important role in carcinogenesis, and in vivo investigations have sho wn increased synthesis of ROS in the gastric mucosa of H.pylori-infected pa tients. In the present study the direct effects of H.pylori on ROS and DNA synthesis, induction of apoptosis and DNA repair were investigated in the g astric epithelial cell lines AGS and HM02. Incubation of gastric cells with H.pylori extract induced the synthesis of ROS, diminished the levels of re duced glutathione (GSH), induced DNA fragmentation and increased DNA synthe sis in gastric cells. Poly(ADP-ribose) formation was increased in gastric c ells exposed to H.pylori extract. FACS analysis of gastric cells exposed to H.pylori extract did not reveal any change in the percentage of cells in t he G(2)/M phase of the cell cycle. The radical scavengers MnTBAP (a cell pe rmeable superoxide dismutase mimic), ebselen (a GSH peroxidase mimic) and h igh doses of catalase completely blocked H.pylori extract-induced elevation in DNA synthesis. Our results indicate that H.pylori extract directly indu ces the synthesis of ROS in gastric epithelial cells and causes DNA damage.