AJP - Gastrointestinal and Liver Physiology, Vol 258, Issue 4 603-G609, Copyright © 1990 by American Physiological Society
Role of oxygen radicals in ethanol-induced damage to cultured gastric mucosal cells
H. Mutoh, H. Hiraishi, S. Ota, K. J. Ivey, A. Terano and T. Sugimoto
Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
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.
