Serum amino acid changes in rats with thioacetamide-induced liver cirrhosis

Fontana, Luis; Moreira, Eliane; Torres, Marı́a Isabel; Fernández, M. Isabel; Rı́os, Antonio; Medina, Fermín Sánchez de; Gil, Ángel

doi:10.1016/0300-483x(95)03177-h

Cited by 75 publications

(57 citation statements)

References 16 publications

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“…Reddy et al (2004) cited that the hepatotoxic compound yields from the binding of TASO2 with tissue macromolecules is responsible for the excessive production of oxidative stress in association with considerable reduction in the glutathione (GSH) pool in the liver. The reduction of intracellular GSH due to TAA administration as shown in the present study has been explained by Fontana et al (1996) as they reported that the active metabolite of TAA can combine with the sulphahydryl groups of proteins resulting in rapid depletion of intracellular GSH concentration. Therefore, the decline of GSH becomes one of the most important Depletion of endogenous GSH leads to overproduction of H2O2 which is very toxic compound and in the presence of transition metal such as iron; it can generate a highly toxic hydroxyl ions that induce lipid peroxidation.…”

Section: Histological Findingssupporting

confidence: 63%

Antifibrotic candidates of Selenium nanoparticles and selenium in the experimental model

2017

J App Pharm Sci

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This research was designed to compare the efficacy of selenium in nanoscale (SeNPs) with its free form (Se) against liver fibrosis induced by thioacetamide (TAA) in rats. In a completely randomized design, 60 adult female rats were distributed as: Group (1) control (received saline) and other three groups received TAA to induce liver fibrosis (100 mg/kg b.wt of three times a week for 6 weeks). Fifteen rats were termed TAA (Group 2). Rats in group (3) were simultaneously administered SeNPs (0.48 mg/kg/b.wt) orally (TAA+SeNPs). Rats in group (4) were simultaneously administered Se (0.48 mg/kg/b.wt) orally (TAA+Se). TAA injection enhanced liver enzymes activity, oxidative stress markers and inflammatory mediators, while suppressed the activity of the antioxidant enzymes activity versus the control group. SeNPs as well as Se supplementation blunted liver enzymes activity, oxidative stress indicators and inflammatory intermediates, while potentiated the activity of the antioxidant enzymes relative to TAA group. Histological investigation of liver tissue appreciated the biochemical findings. Aforementioned data clearly indicate that the mitigation of oxidative stress and inflammation may be the probable mechanisms by which SeNPs or Se can offer their antifibrotic action. Worth mentioning, SeNPs showed superior effect above Se in its free form in this respect.

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Section: Histological Findingssupporting

confidence: 63%

Antifibrotic candidates of Selenium nanoparticles and selenium in the experimental model

2017

J App Pharm Sci

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“…injections into rats produced micronodular cirrhosis (Zimmermann et al 1987;Mori et al 1993;. In addition, the levels of ALP and AST in TA-treated rats increased significantly compared with the control, as previously reported (Fontana et al 1996).…”

Section: Discussionmentioning

confidence: 53%

Immunohistochemical study of macrophage migration inhibitory factor in rat liver fibrosis induced by thioacetamide

Hori

Sato²,

Yamate³

et al. 2009

Eur J Histochem

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Macrophage migration inhibitory factor (MIF) is a molecule known to regulate macrophage accumulation at sites of inflammation. To elucidate the role of MIF in progression of liver fibrosis, the immunohistochemical localization of MIF and macrophages in the liver were examined. Male Wistar rats received thioacetamide (TA) injections (200 mg/kg, i.p.) for 1 or 6 weeks. In biochemical and histological tests, it was confirmed that liver fibrosis was induced. In immunohistochemical analyses, the expression of MIF protein was seen in hepatocytes in the areas extending out from the central veins to the portal tracts. In particular, at 6 weeks, immunoreactivity was detected in degenerated hepatocytes adjacent to the fibrotic areas but hardly observed in the fibrotic areas. On the other hand, a number of exudate macrophages stained by antibody ED1 were seen in the areas from the central veins to the portal tracts at 1 week and in the fibrotic areas at 6 weeks. Macrophages also showed a significant increase in number as compared with controls. These results revealed that there was a close relationship between the appearance of MIF expression and ED1-positive exudate macrophages in degenerated hepatocytes during the progression of TA-induced liver fibrosis

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“…Acute administration of TAA at a high dose to rats induces HE, and this model meets the majority of criteria for type A HE (Zimmerman et al, 1989;Butterworth et al, 2009). On the other hand, chronic TAA treatment at a low dose to rats induces cirrhosis and hepatic tumors (Müller et al, 1988;Fontana et al, 1996;Kawai et al, 2009). The characteristic features of TAA-induced hepatotoxicity in rats resemble those of human cirrhosis (Müller et al, 1988;Dashti et al, 1989;Sato et al, 2000), and rats chronically treated with TAA exhibit memory impairment (Méndez et al, 2008a).…”

Section: Introductionmentioning

confidence: 99%

Behavioral and biochemical characterization of rats treated chronically with thioacetamide: proposal of an animal model for hepatic encephalopathy associated with cirrhosis

et al. 2012

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-Hepatic encephalopathy (HE) is a syndrome observed in patients with liver dysfunction such as hepatitis and cirrhosis, and is characterized by cognitive impairment, personality changes, and a depressed level of consciousness. The detailed mechanism underlying the pathogenesis of HE remains unclear. In the present study, our aim was to establish an animal model for HE with cirrhosis. Therefore, we carried out behavioral and biochemical analysis of cirrhotic rats after treatment with thioacetamide (TAA) for 20 weeks. The rats subjected to chronic TAA treatment (TAA rats) showed reduction of cognitive scores in the novel object recognition test (NOR), and a decrease in immobility and an increase in swimming in the forced swim test (FST). In biochemical analyses, the TAA rats exhibited elevated blood levels of ammonia, and increased metabolic activities of serotonergic and noradrenergic neurons in the brain, while the levels of Glu and GABA were not affected. Post-oral treatment of lactulose, a clinically utilized drug for HE, effectively reduced the elevated blood ammonia levels, and restored the reduced cognitive scores and the decreased immobility, without any effects on neurotransmitter contents in the brain, compared with the control. These results indicated lactulose-restorable memory disturbance and irritated mood in the TAA rats. In other words, rats treated chronically with TAA are a potential model for cirrhosis-HE, and the combination of NOR and FST in TAA rats may be useful as a simple assay system for the screening and development of anti-HE agents.

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Serum amino acid changes in rats with thioacetamide-induced liver cirrhosis

Cited by 75 publications

References 16 publications

Antifibrotic candidates of Selenium nanoparticles and selenium in the experimental model

Antifibrotic candidates of Selenium nanoparticles and selenium in the experimental model

Immunohistochemical study of macrophage migration inhibitory factor in rat liver fibrosis induced by thioacetamide

Behavioral and biochemical characterization of rats treated chronically with thioacetamide: proposal of an animal model for hepatic encephalopathy associated with cirrhosis

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