Mi SciELO
Servicios Personalizados
Revista
Articulo
Indicadores
- Citado por SciELO
- Accesos
Links relacionados
- Citado por Google
- Similares en SciELO
- Similares en Google
Compartir
Nutrición Hospitalaria
versión On-line ISSN 1699-5198versión impresa ISSN 0212-1611
Resumen
GONCALVES SCHEMITT, Elizângela et al. Effect of glutamine on oxidative stress and inflammation in a rat model of fulminant hepatic failure. Nutr. Hosp. [online]. 2016, vol.33, n.2, pp.210-219. ISSN 1699-5198. https://dx.doi.org/10.20960/nh.92.
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.
Palabras clave : Hepatotoxicity; Lipid peroxidation; Antioxidants; Liver; Thioacetamide.