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      Amelioration of thioacetamide-induced liver toxicity in Wistar rats by rutin

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          Abstract

          This study was designed to evaluate the effect of rutin on hepatotoxicity induced by thioacetamide (TAA) in rats. Four groups of male Wistar rats consisting of six rats each were used: Group I: control group; Group II: rats receiving single injection of 300 mg kg −1  body weight of TAA intraperitoneally; Group III: rats administered rutin (10 mg kg −1  body weight) dissolved in saline orally for 2 weeks; and Group IV: rats administered rutin (10 mg kg −1  body weight) dissolved in saline orally for 2 weeks followed by TAA injection last day of second week. All groups were sacrificed after 24 h of treatment and hepatic toxicity was analyzed with respect to liver toxicity markers, liver DNA fragmentation, and histology of liver tissue. Administration of TAA in Wistar rats resulted in significant increase of hepatic markers, DNA fragmentation in the hepatocytes, and changes in histology. Pretreatment of rats with rutin before 2 weeks of TAA assault resulted in the complete reversal of TAA-mediated hepatic toxicity ( P < 0.0001 to P < 0.01) with concomitant restoration of DNA fragmentation. This study suggests rutin as a protective agent for restoration of toxicity caused by TAA.

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          A modification of the Lowry procedure to simplify protein determination in membrane and lipoprotein samples.

          Mary Markwell, Suzanne M. Haas, L.L. Bieber … (1978)
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            Gilbert syndrome and ischemic heart disease: a protective effect of elevated bilirubin levels.

            Libor Vı́tek, Milan Jirsa, Marie Brodanová … (2002)
            Oxidation processes play an important role in atherogenesis. Bilirubin IXalpha is recognised as a potent antioxidant. In the present study, we assessed the role of elevated serum bilirubin levels in the prevention of ischemic heart disease (IHD). The occurrence of IHD was determined in Gilbert syndrome (GS) patients above 40 years (n=50). The diagnosis was based on past medical history and ECG criteria. The occurrence was related to that of the comparable general population (n=2296). Serum biochemistry, including the total antioxidant status was evaluated in the GS subjects, IHD patients (n=38) and control subjects (n=38). The prevalence of IHD in GS subjects (aged 49.7+/-9.0 years) was 2% (0.05-10.7%, 95% confidence interval), compared to 12.1% in a general population (P<0.05). Bilirubin, total antioxidant capacity and high density lipoprotein (HDL) cholesterol were found to be significantly higher in GS subjects compared to control groups (P<0.05). According to linear discriminant analysis, hyperbilirubinemia rather than elevation of HDL cholesterol levels seemed to be more important in protection from IHD. In the present study, low prevalence of IHD in GS subjects was detected. It may be presumed that chronic hyperbilirubinemia prevent the development of IHD by increasing the serum antioxidant capacity.
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              Current Concepts of Mechanisms in Drug-Induced Hepatotoxicity

              Stefan Russmann, Gerd Kullak-Ublick, Ignazio Grattagliano (2009)
              Drug-induced liver injury (DILI) has become a leading cause of severe liver disease in Western countries and therefore poses a major clinical and regulatory challenge. Whereas previously drug-specific pathways leading to initial injury of liver cells were the main focus of mechanistic research and classifications, current concepts see these as initial upstream events and appreciate that subsequent common downstream pathways and their attenuation by drugs and other environmental and genetic factors also have a profound impact on the risk of an individual patient to develop overt liver disease. This review summarizes current mechanistic concepts of DILI in a 3-step model that limits its principle mechanisms to three main ways of initial injury, i.e. direct cell stress, direct mitochondrial impairment, and specific immune reactions. Subsequently, initial injury initiates further downstream events, i.e. direct and death receptor-mediated pathways leading to mitochondrial permeability transition, which then results in apoptotic or necrotic cell death. For all mechanisms, mitochondria play a central role in events leading to apoptotic vs. necrotic cell death. New treatment targets consequently focus on interference with downstream pathways that mediate injury and therefore determine the ultimate outcome of DILI. Genome wide and targeted pharmacogenetic as well as metabonomic approaches are now used in order to reach the key goals of a better understanding of mechanisms in hepatotoxicity, and to develop new strategies for its prediction and treatment. However, the complexity of interactions between genetic and environmental risk factors is considerable, and DILI therefore currently remains unpredictable for most hepatotoxins.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Immunopathol Pharmacol
                Journal ID (iso-abbrev): Int J Immunopathol Pharmacol
                Journal ID (publisher-id): IJI
                Journal ID (hwp): spiji
                Title: International Journal of Immunopathology and Pharmacology
                Publisher: SAGE Publications (Sage UK: London, England )
                ISSN (Print): 0394-6320
                ISSN (Electronic): 2058-7384
                Publication date (Electronic): 07 June 2017
                Publication date (Print): September 2017
                Volume: 30
                Issue: 3
                Pages: 207-214
                Affiliations
                [1 ]Biochemistry Department, College of Sciences, King Saud University, Riyadh, Saudi Arabia
                [2 ]Pharmaceutical Chemistry Department, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia
                [3 ]Department of Pharmacology, College of Pharmacy, Prince Sattam Bin Abdulaziz University, Al Kharj, Saudi Arabia
                Author notes
                [*]Seema Zargar, Biochemistry Department, College of Sciences, King Saud University, Riyadh 11495, Saudi Arabia. Email: szargar@ 123456ksu.edu.sa
                Article
                Publisher ID: 10.1177_0394632017714175
                DOI: 10.1177/0394632017714175
                PMC ID: 5815265
                PubMed ID: 28590141
                SO-VID: ca0c700c-4cfc-4d2d-9667-79ea4b7c543e
                Copyright © © The Author(s) 2017
                License:

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                Date received : 21 March 2017
                Date accepted : 21 April 2017
                Categories
                Subject: Original Research Articles

                Keywords: liver enzymes,oxidative stress,rutin,thioacetamide,toxicity
                Data availability:
                Keywords: liver enzymes, oxidative stress, rutin, thioacetamide, toxicity

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