Acetyl salicylic acid-induced gastric mucosal lesions: no role of gastric glutathione.
Gastric glutathione (GSH) depletion has been implicated in the causation of gastric mucosal lesions by ethanol, diethylmaleate (DEM) and acrylonitrile (VCN). The purpose of the current studies was to investigate the role of gastric GSH in Acetyl Salicylic acid (Aspirin; ASA) induced gastric lesions. Intragastric administration of doses of ASA to rats, which caused gastric mucosal lesions, had no significant influence on gastric or hepatic GSH concentrations. Furthermore, pretreatment of rats with sulfhydryl-containing chemicals (e.g. L-cysteine) failed to protect against the ASA- or Acid-induced gastric lesions. Our findings indicate that gastric GSH plays no role in the pathogenesis of ASA-induced gastric mucosal necrosis.
D000818:Animals; D001241:Aspirin / Q000494:pharmacology*; D003545:Cysteine / Q000494:pharmacology; D005744:Gastric Acid / Q000378:metabolism; D005753:Gastric Mucosa / Q000187:drug effects*; D005978:Glutathione / Q000378:metabolism*; D008099:Liver / Q000378:metabolism; D008297:Male; D009336:Necrosis / Q000139:chemically induced; D051381:Rats; D011919:Rats, Inbred Strains
D005978:Glutathione; D003545:Cysteine; D001241:Aspirin