Document Detail


Glutamine prevents gastric oxidative stress in an animal model of portal hypertension gastropathy.
MedLine Citation:
PMID:  21911895     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Camila Marques; José L Mauriz; Douglas Simonetto; Claudio A Marroni; María J Tuñon; Javier González-Gallego; Norma P Marrón
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Annals of hepatology     Volume:  10     ISSN:  1665-2681     ISO Abbreviation:  Ann Hepatol     Publication Date:    2011 Oct-Dec
Date Detail:
Created Date:  2011-09-13     Completed Date:  2011-11-23     Revised Date:  2013-05-16    
Medline Journal Info:
Nlm Unique ID:  101155885     Medline TA:  Ann Hepatol     Country:  Mexico    
Other Details:
Languages:  eng     Pagination:  531-9     Citation Subset:  IM    
Affiliation:
Universidade Federal do Rio Grande do Sul-UFRGS. Brazil.
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MeSH Terms
Descriptor/Qualifier:
Alanine Transaminase / blood
Alkaline Phosphatase / blood
Animals
Antioxidants / pharmacology*
Aspartate Aminotransferases / blood
Biological Markers / blood,  metabolism
Catalase / metabolism
Disease Models, Animal
Glutamine / pharmacology*
Glutathione Peroxidase / metabolism
Hypertension, Portal / complications,  drug therapy*,  metabolism
Ligation
Lipid Peroxidation / drug effects
Male
Nitric Oxide / metabolism
Oxidative Stress / drug effects*
Portal Vein / surgery
Rats
Rats, Wistar
Stomach / drug effects*,  metabolism,  pathology
Stomach Diseases / etiology,  metabolism,  pathology,  prevention & control*
Superoxide Dismutase / metabolism
Thiobarbituric Acid Reactive Substances / metabolism
Chemical
Reg. No./Substance:
0/Antioxidants; 0/Biological Markers; 0/Thiobarbituric Acid Reactive Substances; 10102-43-9/Nitric Oxide; 56-85-9/Glutamine; EC 1.11.1.6/Catalase; EC 1.11.1.9/Glutathione Peroxidase; EC 1.15.1.1/Superoxide Dismutase; EC 2.6.1.1/Aspartate Aminotransferases; EC 2.6.1.2/Alanine Transaminase; EC 3.1.3.1/Alkaline Phosphatase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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