Protection by zinc sulphate against ethanol-induced ulceration: preservation of the gastric mucosal barrier.

Abstract

The aetiology of ethanol-induced gastric ulceration, and its interaction with zinc, were studied in rats. Oral administration of ethanol (40, 50 or 80%) to conscious rats reduced the stomach mucus content and increased gastric ulcer formation in a concentration-dependent manner. Histological examination indicated that mucus, both on the surface and within the epithelium, was depleted because of epithelium being shed from the gastric mucosa. Zinc sulphate abolished mucus loss and ulcer formation in the ethanol-treated animals. Using an ex-vivo gastric chamber preparation in anaesthetised animals, it was found that an ethanol (50%)-HCl (100 mmol/l) solution produced severe glandular haemorrhagic ulceration, elevated Na+, K+ and protein levels in the luminal solution, and reduced the H+ content in this fluid. Zinc sulphate pretreatment dose-dependently prevented all these changes. On the other hand, prostaglandin E2 (PGE2) administration only antagonised ethanol ulceration and H+ loss from the chamber; it did not significantly influence the Na+ and K+ fluxes and protein leakage into the luminal solution. It is concluded that the antiulcer mechanisms of zinc sulphate and PGE2 may be different. Protection by the former drug could be due partly to preservation of mucus adhering to the gastric mucosa. The possibility of the membrane-stabilising action of zinc contributing to the observed effects is also discussed.