Role of oxidative stress in lansoprazole-mediated gastric and hepatic protection in Wistar rats.

BACKGROUND AND AIM Lansoprazole, a benzimidazole derivative, is a widely-used proton-pump inhibitor. In addition, it has been reported to have an independent gastroprotective action. Since free radicals and antioxidant mechanisms appear to counter-act tissue-related injury, we studied the effect of lansoprazole on oxidative stress in acid-ethanol gastric injury. As this drug is metabolized in the liver, we also studied its effect on the liver. METHODS Wistar rats were divided into three groups: control group, group I (vehicle treatment) and group II (lansoprazole treatment for eight days). In all the groups, injury was induced by ethanol-HCl administration. The effect of lansoprazole on free-radical generation and various antioxidants, e.g. superoxide dismutase (SOD), catalase, reduced glutathione (GSH), glutathione-s-transferase (GST) and glutathione reductase was evaluated in the gastric mucosal and liver homogenates. RESULTS Ethanol-HCl administration initiated injury as shown by increase in malondialdehyde (MDA) levels in both gastric mucosa and liver. There was an increase in SOD and GST activity and a decrease in catalase, glutathione reductase and GSH in the gastric mucosa. In liver, ethanol-HCl administration decreased the activity of SOD, catalase and GSH and increased GST activity. Lansoprazole pretreatment led to decrease in the levels of MDA and increase in SOD, catalase, GSH, glutathione reductase and GST in both the gastric mucosa and liver. CONCLUSIONS Lansoprazole has a protective action on gastric mucosa and the liver. This protection is mediated by a decrease in oxidative stress and a concomitant in-crease in antioxidants.