TY - JOUR
T1 - Glutamine prevents gastric oxidative stress in an animal model of portal hypertension gastropathy
AU - Marques, Camila
AU - Mauriz, José L.
AU - Simonetto, Douglas
AU - Marroni, Claudio A.
AU - Tuñon, María J.
AU - González-Gallego, Javier
AU - Marrón, Norma P.
N1 - Funding Information:
We would like to thank to Maria Angeles Busturia, Yeray Duque, Ascensión Valle and Eunate Arana for their clinical and technical help and thanks to Julia G Fenn (INC team) and Alejandro Urberuaga for their English translation. The study was financially supported by the Department of Health and Department of Education of the Government of the Basque Country (research grant: 200211011 , IT-472-07 ), Fundación Salud 2000 , Grant number 23301 and Fundación IKERTU . We extend our gratitude to the Sociedad Española de Endocrinología Pediátrica for the award “José Igea 2002” funded by Pfizer . Finally, we want to thank the children and their parents for their continued participation and involvement in this research.
PY - 2011
Y1 - 2011
N2 - 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.
AB - 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.
KW - Glutamine
KW - Nitric oxide
KW - Portal hypertension
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U2 - 10.1016/s1665-2681(19)31522-4
DO - 10.1016/s1665-2681(19)31522-4
M3 - Article
C2 - 21911895
AN - SCOPUS:80052866449
SN - 1665-2681
VL - 10
SP - 531
EP - 539
JO - Annals of hepatology
JF - Annals of hepatology
IS - 4
ER -