Effect of glutamine on oxidative stress and inflammation in a rat model of fulminant hepatic failure

Introduction: Fulminant hepatic failure (FHF) is a rare clinical syndrome, characterized by sudden and severe liver dysfunction. Thioacetamide (TAA) is a hepatotoxin whose administration can induce centrilobular necrosis in liver cells and increase the formation of reactive oxygen species and lipid peroxidation in rats. Glutamine is a precursor for glutathione synthesis. Objective: The objective of the study to assess the antioxidant effects of glutamine in a rat model of TAA-induced FHF. Methods: Male Wistar rats were divided into four groups according to treatment and time of assessment: control, glutamine (25 mg/kg), thioacetamide (400 mg/kg) and thioacetamide plus glutamine. Animals were assessed after 24, 36 and 48 hours. Blood samples were collected for the analysis of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AP), total bilirubin (TB) and creatinine (CRE) levels, and liver samples were used to evaluate lipid peroxidation, acid-reactive thiobarbituric substances (TBARS), antioxidant enzyme activity superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and glutathione S-transferase (GST). Nuclear factor κB (NF-κB), tumor necrosis factors (TNF-α) and nitric oxide synthase inducible (iNOS) levels were assessed by histology and immunohistochemistry. Results: TAA caused alterations in biochemical and histological parameters, and increased markers of the inflammatory process. TBARS levels and the activity of SOD and GST were significantly lower in the glutamine group as compared to the TAA group. CAT activity was elevated in animals treated with glutamine as compared to the TAA groups. GPx activity was also lower in the glutamine-treated groups than in TAA-treated animals at 36 and 48 hours. Tissue damage and NF-κB, TNF-α and iNOS expression were significantly lower in animals treated with glutamine. Conclusion: Glutamine has shown to have protective effects against liver damage in a rat model of TAA-induced FHF.

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Main Authors: Gonçalves Schemitt,Elizângela, Raskopf Colares,Josieli, Minuzzo Hartmann,Renata, Morgan-Martins,María Isabel, Marroni,Cláudio Augusto, Tuñón,M. Jesús, Possa Marroni,Norma
Format: Digital revista
Language:English
Published: Grupo Arán 2016
Online Access:http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S0212-16112016000200004
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spelling oai:scielo:S0212-161120160002000042016-09-21Effect of glutamine on oxidative stress and inflammation in a rat model of fulminant hepatic failureGonçalves Schemitt,ElizângelaRaskopf Colares,JosieliMinuzzo Hartmann,RenataMorgan-Martins,María IsabelMarroni,Cláudio AugustoTuñón,M. JesúsPossa Marroni,Norma Hepatotoxicity Lipid peroxidation Antioxidants Liver Thioacetamide Introduction: Fulminant hepatic failure (FHF) is a rare clinical syndrome, characterized by sudden and severe liver dysfunction. Thioacetamide (TAA) is a hepatotoxin whose administration can induce centrilobular necrosis in liver cells and increase the formation of reactive oxygen species and lipid peroxidation in rats. Glutamine is a precursor for glutathione synthesis. Objective: The objective of the study to assess the antioxidant effects of glutamine in a rat model of TAA-induced FHF. Methods: Male Wistar rats were divided into four groups according to treatment and time of assessment: control, glutamine (25 mg/kg), thioacetamide (400 mg/kg) and thioacetamide plus glutamine. Animals were assessed after 24, 36 and 48 hours. Blood samples were collected for the analysis of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AP), total bilirubin (TB) and creatinine (CRE) levels, and liver samples were used to evaluate lipid peroxidation, acid-reactive thiobarbituric substances (TBARS), antioxidant enzyme activity superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and glutathione S-transferase (GST). Nuclear factor κB (NF-κB), tumor necrosis factors (TNF-α) and nitric oxide synthase inducible (iNOS) levels were assessed by histology and immunohistochemistry. Results: TAA caused alterations in biochemical and histological parameters, and increased markers of the inflammatory process. TBARS levels and the activity of SOD and GST were significantly lower in the glutamine group as compared to the TAA group. CAT activity was elevated in animals treated with glutamine as compared to the TAA groups. GPx activity was also lower in the glutamine-treated groups than in TAA-treated animals at 36 and 48 hours. Tissue damage and NF-κB, TNF-α and iNOS expression were significantly lower in animals treated with glutamine. Conclusion: Glutamine has shown to have protective effects against liver damage in a rat model of TAA-induced FHF.Grupo AránNutrición Hospitalaria v.33 n.2 20162016-04-01journal articletext/htmlhttp://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S0212-16112016000200004en
institution SCIELO
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country España
countrycode ES
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libraryname SciELO
language English
format Digital
author Gonçalves Schemitt,Elizângela
Raskopf Colares,Josieli
Minuzzo Hartmann,Renata
Morgan-Martins,María Isabel
Marroni,Cláudio Augusto
Tuñón,M. Jesús
Possa Marroni,Norma
spellingShingle Gonçalves Schemitt,Elizângela
Raskopf Colares,Josieli
Minuzzo Hartmann,Renata
Morgan-Martins,María Isabel
Marroni,Cláudio Augusto
Tuñón,M. Jesús
Possa Marroni,Norma
Effect of glutamine on oxidative stress and inflammation in a rat model of fulminant hepatic failure
author_facet Gonçalves Schemitt,Elizângela
Raskopf Colares,Josieli
Minuzzo Hartmann,Renata
Morgan-Martins,María Isabel
Marroni,Cláudio Augusto
Tuñón,M. Jesús
Possa Marroni,Norma
author_sort Gonçalves Schemitt,Elizângela
title Effect of glutamine on oxidative stress and inflammation in a rat model of fulminant hepatic failure
title_short Effect of glutamine on oxidative stress and inflammation in a rat model of fulminant hepatic failure
title_full Effect of glutamine on oxidative stress and inflammation in a rat model of fulminant hepatic failure
title_fullStr Effect of glutamine on oxidative stress and inflammation in a rat model of fulminant hepatic failure
title_full_unstemmed Effect of glutamine on oxidative stress and inflammation in a rat model of fulminant hepatic failure
title_sort effect of glutamine on oxidative stress and inflammation in a rat model of fulminant hepatic failure
description Introduction: Fulminant hepatic failure (FHF) is a rare clinical syndrome, characterized by sudden and severe liver dysfunction. Thioacetamide (TAA) is a hepatotoxin whose administration can induce centrilobular necrosis in liver cells and increase the formation of reactive oxygen species and lipid peroxidation in rats. Glutamine is a precursor for glutathione synthesis. Objective: The objective of the study to assess the antioxidant effects of glutamine in a rat model of TAA-induced FHF. Methods: Male Wistar rats were divided into four groups according to treatment and time of assessment: control, glutamine (25 mg/kg), thioacetamide (400 mg/kg) and thioacetamide plus glutamine. Animals were assessed after 24, 36 and 48 hours. Blood samples were collected for the analysis of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AP), total bilirubin (TB) and creatinine (CRE) levels, and liver samples were used to evaluate lipid peroxidation, acid-reactive thiobarbituric substances (TBARS), antioxidant enzyme activity superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and glutathione S-transferase (GST). Nuclear factor κB (NF-κB), tumor necrosis factors (TNF-α) and nitric oxide synthase inducible (iNOS) levels were assessed by histology and immunohistochemistry. Results: TAA caused alterations in biochemical and histological parameters, and increased markers of the inflammatory process. TBARS levels and the activity of SOD and GST were significantly lower in the glutamine group as compared to the TAA group. CAT activity was elevated in animals treated with glutamine as compared to the TAA groups. GPx activity was also lower in the glutamine-treated groups than in TAA-treated animals at 36 and 48 hours. Tissue damage and NF-κB, TNF-α and iNOS expression were significantly lower in animals treated with glutamine. Conclusion: Glutamine has shown to have protective effects against liver damage in a rat model of TAA-induced FHF.
publisher Grupo Arán
publishDate 2016
url http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S0212-16112016000200004
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