Glutamine prevents gastric oxidative stress in an animal model of portal hypertension gastropathy

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

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

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 peroxidase (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.

Original languageEnglish (US)
Pages (from-to)531-539
Number of pages9
JournalAnnals of Hepatology
Volume10
Issue number4
StatePublished - Sep 21 2011
Externally publishedYes

Fingerprint

Portal Hypertension
Glutamine
Stomach
Oxidative Stress
Animal Models
Portal Vein
Superoxide Dismutase
Ligation
Nitric Oxide
Thiobarbituric Acid Reactive Substances
Transaminases
Alkaline Phosphatase
Antioxidants
Portal System
Portal Pressure
Glutathione Peroxidase
Gastric Mucosa
Luminescence
Vasodilation
Vascular Resistance

Keywords

  • Glutamine
  • Nitric oxide
  • Portal hypertension

ASJC Scopus subject areas

  • Hepatology

Cite this

Marques, C., Mauriz, J. L., Simonetto, D., Marroni, C. A., Tuñon, M. J., González-Gallego, J., & Marrón, N. P. (2011). Glutamine prevents gastric oxidative stress in an animal model of portal hypertension gastropathy. Annals of Hepatology, 10(4), 531-539.

Glutamine prevents gastric oxidative stress in an animal model of portal hypertension gastropathy. / Marques, Camila; Mauriz, José L.; Simonetto, Douglas; Marroni, Claudio A.; Tuñon, María J.; González-Gallego, Javier; Marrón, Norma P.

In: Annals of Hepatology, Vol. 10, No. 4, 21.09.2011, p. 531-539.

Research output: Contribution to journalArticle

Marques, C, Mauriz, JL, Simonetto, D, Marroni, CA, Tuñon, MJ, González-Gallego, J & Marrón, NP 2011, 'Glutamine prevents gastric oxidative stress in an animal model of portal hypertension gastropathy', Annals of Hepatology, vol. 10, no. 4, pp. 531-539.
Marques C, Mauriz JL, Simonetto D, Marroni CA, Tuñon MJ, González-Gallego J et al. Glutamine prevents gastric oxidative stress in an animal model of portal hypertension gastropathy. Annals of Hepatology. 2011 Sep 21;10(4):531-539.
Marques, Camila ; Mauriz, José L. ; Simonetto, Douglas ; Marroni, Claudio A. ; Tuñon, María J. ; González-Gallego, Javier ; Marrón, Norma P. / Glutamine prevents gastric oxidative stress in an animal model of portal hypertension gastropathy. In: Annals of Hepatology. 2011 ; Vol. 10, No. 4. pp. 531-539.
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