title: Glutamine prevents gastric oxidative stress in an animal model of portal hypertension gastropathy.
abstract: OBJECTIVE
  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).
  
  
  OBJECTIVE
  To investigate the effects of glutamine on oxidative stress in an experimental model of PHG induced by partial portal vein ligation (PPVL).
  
  
  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.
authors.affiliation: Universidade Federal do Rio Grande do Sul-UFRGS. Brazil.
authors.forename: Camila
authors.initials: C
authors.lastname: Marques
authors.forename: José L
authors.initials: JL
authors.lastname: Mauriz
authors.forename: Douglas
authors.initials: D
authors.lastname: Simonetto
authors.forename: Claudio A
authors.initials: CA
authors.lastname: Marroni
authors.forename: María J
authors.initials: MJ
authors.lastname: Tuñon
authors.forename: Javier
authors.initials: J
authors.lastname: González-Gallego
authors.forename: Norma P
authors.initials: NP
authors.lastname: Marrón
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000469:Alkaline Phosphatase / Q000097:blood; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001219:Aspartate Aminotransferases / Q000097:blood; D015415:Biomarkers / Q000097:blood / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D004195:Disease Models, Animal; D005753:Gastric Mucosa / Q000378:metabolism; D005973:Glutamine / Q000494:pharmacology*; D005979:Glutathione Peroxidase / Q000378:metabolism; D006975:Hypertension, Portal / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism; D008026:Ligation; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D011169:Portal Vein / Q000601:surgery; D051381:Rats; D017208:Rats, Wistar; D013270:Stomach / Q000187:drug effects* / Q000473:pathology; D013272:Stomach Diseases / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D017392:Thiobarbituric Acid Reactive Substances; D005973:Glutamine; D009569:Nitric Oxide; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D000469:Alkaline Phosphatase