Gastric mucosal oxidation of ethanol is not involved in ethanol-induced mucosal damage.
The involvement of gastric mucosal metabolism of ethanol in ethanol-induced mucosal damage was studied in urethane anaesthetised rats. Pyrazole, an inhibitor of alcohol dehydrogenase (ADH), slightly aggravated the mucosal lesions produced by intragastric instillation of 30% (v/v) ethanol, but had no effect on increased mucosal permeability to ions, pepsinogen and fluid output or on gastric mucosal blood flow associated with mucosal injury. Induction of ADH by ethanol pre-treatment had no effect on the above-mentioned parameters. Intragastric instillation of acetaldehyde, the product of ethanol oxidation, did not cause lesions in the gastric mucosa. The results suggest that the gastric mucosal toxicity of ethanol may not be related to its metabolism in the gastric mucosa.
D000079:Acetaldehyde / Q000633:toxicity; D000818:Animals; D000431:Ethanol / Q000378:metabolism* / Q000633:toxicity; D005753:Gastric Mucosa / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism*; D006863:Hydrogen-Ion Concentration; D008297:Male; D010084:Oxidation-Reduction; D011720:Pyrazoles / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012039:Regional Blood Flow / Q000187:drug effects
D011720:Pyrazoles; D000431:Ethanol; C031280:pyrazole; D000079:Acetaldehyde