Annals of Hepatology (Oct 2011)

Glutamine prevents gastric oxidative stress in an animal model of portal hypertension gastropathy(◆)(◆)This work was supported by grants from the Conselho Nacional de Desenvolvimiento Científico e Tecnológico (CNPq), Fundaçáo de Amparo a Pesquisa do Rio Grande do Sul (FAPERGS), and Fundo de Incentivo á Pesquisa e Eventos (FIPE) do Hospital de Clínicas de Porto Alegre (HCPA). CIBEREHD is funded by the Instituto de Salud Carlos III.

  • Camila Marques,
  • José L. Mauriz,
  • Douglas Simonetto,
  • Claudio A. Marroni,
  • María J. Tuñon,
  • Javier González-Gallego,
  • Norma P. Marroni

Journal volume & issue
Vol. 10, no. 4
pp. 531 – 539

Abstract

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Background and rationale. Portal hypertension (PHI) is a clinical syndrome characterized by increases of the blood flow and/or of the vascular resistance in the portal system. A direct consequence of PHI can appearance different lesions on the gastric mucosa and submucosa, cumulatively termed portal hypertensive gastropathy (PHG). Aims. To investigate the effects of glutamine on oxidative stress in an experimental model of PHG induced by partial portal vein ligation (PPVL).Material and methods. Portal pressure, transaminase and alkaline phosphatase activity were quantified. Gastric tissue damage was assessed by histological analysis. Oxidative stress was measured by quantification of cytosolic concentration of thiobarbituric acid reactive substances (TBARS), hydroperoxide-initiated chemiluminescence (QL), and nitric oxide (NO) production. Moreover, activities of the antioxidant enzymes superoxide dismutase (SOD), glutathione pe-roxidase (GPx), and catalase (CAT) were analyzed.Results. Transaminase and alkaline phosphatase activities were not significantly modified by PPVL, indicating absence of liver injury. Histological analysis of gastric sections showed a lost of normal architecture, with edema and vasodilatation. TBARS, QL, and NO production were significantly increased in PPVL animals. A reduction of SOD activity was found. Glutamine administration markedly alleviated histological abnormalities and oxidative stress, normalized SOD activity, and blocked NO overproduction.Conclusions. Our results confirm that the use of molecules with antioxidant capacity can provide protection of the gastric tissue in portal hypertension. Glutamine treatment can be useful to reduce the oxidative damage induced by PHI on gastric tissue.

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