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Leke R.,Federal University of Rio Grande do Sul | Leke R.,Experimental Hepatology and Gastroenterology Laboratory | de Oliveira D.L.,Federal University of Rio Grande do Sul | Mussulini B.H.M.,Federal University of Rio Grande do Sul | And 11 more authors.
PLoS ONE | Year: 2012

Hepatic encephalopathy (HE) arises from acute or chronic liver diseases and leads to several problems, including motor impairment. Animal models of chronic liver disease have extensively investigated the mechanisms of this disease. Impairment of locomotor activity has been described in different rat models. However, these studies are controversial and the majority has primarily analyzed activity parameters. Therefore, the aim of the present study was to evaluate locomotor and exploratory behavior in bile duct-ligated (BDL) rats to explore the spatial and temporal structure of behavior. Adult female Wistar rats underwent common bile duct ligation (BDL rats) or the manipulation of common bile duct without ligation (control rats). Six weeks after surgery, control and BDL rats underwent open-field, plus-maze and foot-fault behavioral tasks. The BDL rats developed chronic liver failure and exhibited a decrease in total distance traveled, increased total immobility time, smaller number of rearings, longer periods in the home base area and decreased percentage of time in the center zone of the arena, when compared to the control rats. Moreover, the performance of the BDL rats was not different from the control rats for the elevated plus-maze and foot-fault tasks. Therefore, the BDL rats demonstrated disturbed spontaneous locomotor and exploratory activities as a consequence of altered spatio-temporal organization of behavior. © 2012 Leke et al.

Schemitt E.G.,Federal University of Rio Grande do Sul | Schemitt E.G.,Experimental Hepatology and Gastroenterology Laboratory | Schemitt E.G.,Oxidative Stress and Antioxidants Laboratory | Colares J.R.,Lutheran University of Brazil | And 13 more authors.
Nutricion Hospitalaria | Year: 2016

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 kB (NF-kB), 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-kB, TNF-a 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. © 2016, Grupo Aula Medica S.A. All rights reserved.

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