Acetyl salicylic acid-induced gastric mucosal lesions: No role of gastric glutathione

B. I. Ghanayem, A. E. Ahmed, P. J. Boor

Research output: Contribution to journalArticle

8 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)153-156
Number of pages4
JournalResearch Communications in Chemical Pathology and Pharmacology
Volume45
Issue number1
StatePublished - Jan 1 1984

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Toxicology
  • Pharmacology
  • Pharmacology, Toxicology and Pharmaceutics(all)

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