Role of oxygen radicals in ethanol-induced damage to cultured gastric mucosal cells

We have examined the role of oxygen radicals in ethanol-induced damage to cultured rat gastric mucosal cells. Cultured cells exposed to ethanol produced superoxide anion, as assessed by the reduction of cytochrome c, in a time-related fashion. The production of superoxide anion increased dose dependently as the concentration of ethanol increased. Cellular damage increased in a similar fashion to the production of superoxide anion. Both superoxide dismutase (SOD) and catalase diminished ethanol-induced injury dose dependently. SOD and catalase were able to maintain their enzymatic activities in the presence of 15% ethanol, respectively. Pretreatment with deferoxamine, an iron-chelating agent, decreased ethanol-induced injury dose dependently. Furthermore, dimethyl sulfoxide decreased ethanol-induced damage dose dependently. We conclude that cultured gastric mucosal cells exposed to ethanol generate oxygen radicals and that the production of oxygen radicals is closely linked with ethanol-induced damage to the cells. Hydroxyl radical, produced by the iron-catalyzed Haber-Weiss reaction, seems to be the main mediator of ethanol-induced damage to gastric mucosal cells in vitro.