Protective effect of zinc gluconate on chemically induced gastric ulcer.

This study was undertaken in rats to ascertain the role of zinc as an antiulcerogenic agent employing its more bioavailable gluconate derivative. Pretreatment with zinc gluconate 10 mg/kg body wt orally for three consecutive days, protected against alcohol induced gastric epithelial damage and also significantly prevented non-steroidal anti-inflammatory drugs (NSAID) induced gastric ulcer in rats. The enhanced levels of mucus, and hexosamine and decreased acid output in the gastric secretion of zinc treated rats, increased the gastric mucosal barrier. Studies on the mechanism of action suggested the involvement of -SH groups in producing gastric antisecretory effect. Thus, zinc gluconate at > > 100 microM concentrations inhibited H(+)-ion transport which could be reversed by incorporating beta-mercaptoethanol in the secretory solution (luminal side). On the other hand, beta-mercaptoethanol added from the nutrient side showed no effect on the inhibition of H(+)-transport indicting that the implication of -SH groups may not be the sole factor. Zinc appeared to play a vital and multifaceted protective role in chemically induced gastric ulcer disorders.