Digestive Diseases and Sciences

, Volume 44, Issue 7, pp 1417–1422

Nitric Oxide-Mediated Regulation of Gastric H+, K+-ATPase and Alcohol Dehydrogenase Following Ethanol-Induced Injury in Rats

  • Authors
  • R. Bulut
  • Y. Unlucerci
  • S. Bekpinar
  • L. Kuntsal

DOI: 10.1023/A:1026608020133

Cite this article as:
Bulut, R., Unlucerci, Y., Bekpinar, S. et al. Dig Dis Sci (1999) 44: 1417. doi:10.1023/A:1026608020133


The mucosal protective effect of nitric oxide(NO) was examined by usingNG-nitro-L-arginine methyl ester (L-NAME) asnitric oxide synthase (NOS) inhibitor and nitroprusside(NP) as NO donating agent, in ethanol-induced rat gastric lesion model.The results are summarized as follows: (1) As gastrictissue samples were examined by light microscopy,intragastric exposure of ethanol was demonstrated to induce gastric injury, which was more prominentin female rats. The depletion of NO by L-NAME treatmentexacerbated the ethanol-induced gastric lesion but NPtogether with ethanol promoted repair of the mucosal injury, especially in female rats. (2)Gastric H+, K+-ATPase enzymeactivity, which was responsible for acid secretion,seemed not to be effected by ethanol treatment. Togetherwith ethanol, L-NAME treatment activated, whereas NP treatmentinhibited, the enzyme activity in female rats. (3)Ethanol treatment inhibited gastric alcoholdehydrogenase (ADH) activity, which was responsible forthe first-pass metabolism of ethanol. Together with ethanol,L-NAME did not effect the enzyme activity whereas NPtreatment disappeared the inhibitory effect of ethanolin both gender. Hydroxyl radical (OH•) scavenger activity was found to increase in ethanol andethanol + NP groups in both sexes, but superoxideradical (O2-•) scavengeractivity did not change. The results indicate that NOmay ameliorate the damaging effect of ethanol possibly by regulating acidsecretion, ethanol metabolism, and antioxidant contentin rat gastric mucosa.


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© Plenum Publishing Corporation 1999