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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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 |
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Gonçalves Schemitt,Elizângela Raskopf Colares,Josieli Minuzzo Hartmann,Renata Morgan-Martins,María Isabel Marroni,Cláudio Augusto Tuñón,M. Jesús Possa Marroni,Norma |
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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. |
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Grupo Arán |
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2016 |
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http://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S0212-16112016000200004 |
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