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Efficacy of caffeic acid in preventing nickel induced oxidative damage in liver of rats.

Abstract

Nickel (Ni), a major environmental pollutant, is known for its wide toxic manifestations. In the present study caffeic acid (CA), one of the most commonly occurring phenolic acids in fruits, grains and dietary supplements, was evaluated for its protective effect against the Ni induced oxidative damage in liver. In this investigation, Ni (20 mg/kg body weight) was administered intraperitoneally for 20 days to induce toxicity. CA was administered orally (15, 30 and 60 mg/kg body weight) for 20 days with intraperitoneal administration of Ni. Ni induced liver damage was clearly shown by the increased activities of serum hepatic enzymes namely aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), gamma glutamyl transferase (GGT) and lactate dehydrogenase (LDH) along with increased elevation of lipid peroxidation indices (thiobarbituric reactive acid substances (TBARS) and lipid hydroperoxides). The toxic effect of Ni was also indicated by significantly decreased levels of enzymatic (superoxide dismutase (SOD), catalase (CAT) glutathione peroxidase (GPx) and glutathione S-transferase (GST)) and non-enzymatic antioxidants (glutathione (GSH), vitamin C and vitamin E). CA administered at a dose of 60 mg/kg body weight significantly reversed the activities of hepatic marker enzymes to their near normal levels when compared with other two doses. In addition, CA significantly reduced lipid peroxidation and restored the levels of antioxidant defense in the liver. All these changes were supported by histological observations. The results indicate that CA may be beneficial in ameliorating the Ni induced oxidative damage in the liver of rats.

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  • Authors+Show Affiliations

    ,

    Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalainagar 608002, Tamilnadu, India. paribalaji@gmail.com

    Source

    Chemico-biological interactions 173:2 2008 May 28 pg 77-83

    MeSH

    Alanine Transaminase
    Alkaline Phosphatase
    Animals
    Antioxidants
    Aspartate Aminotransferases
    Caffeic Acids
    Catalase
    Chemical and Drug Induced Liver Injury
    Glutathione Peroxidase
    Glutathione Transferase
    L-Lactate Dehydrogenase
    Liver
    Liver Diseases
    Male
    Nickel
    Random Allocation
    Rats
    Rats, Wistar
    Superoxide Dismutase
    Thiobarbituric Acid Reactive Substances
    gamma-Glutamyltransferase

    Pub Type(s)

    Journal Article

    Language

    eng

    PubMed ID

    18405891

    Citation

    Pari, L, and A Prasath. "Efficacy of Caffeic Acid in Preventing Nickel Induced Oxidative Damage in Liver of Rats." Chemico-biological Interactions, vol. 173, no. 2, 2008, pp. 77-83.
    Pari L, Prasath A. Efficacy of caffeic acid in preventing nickel induced oxidative damage in liver of rats. Chem Biol Interact. 2008;173(2):77-83.
    Pari, L., & Prasath, A. (2008). Efficacy of caffeic acid in preventing nickel induced oxidative damage in liver of rats. Chemico-biological Interactions, 173(2), pp. 77-83. doi:10.1016/j.cbi.2008.02.010.
    Pari L, Prasath A. Efficacy of Caffeic Acid in Preventing Nickel Induced Oxidative Damage in Liver of Rats. Chem Biol Interact. 2008 May 28;173(2):77-83. PubMed PMID: 18405891.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Efficacy of caffeic acid in preventing nickel induced oxidative damage in liver of rats. AU - Pari,L, AU - Prasath,A, Y1 - 2008/03/06/ PY - 2007/12/17/received PY - 2008/02/26/revised PY - 2008/02/27/accepted PY - 2008/4/15/pubmed PY - 2008/7/9/medline PY - 2008/4/15/entrez SP - 77 EP - 83 JF - Chemico-biological interactions JO - Chem. Biol. Interact. VL - 173 IS - 2 N2 - Nickel (Ni), a major environmental pollutant, is known for its wide toxic manifestations. In the present study caffeic acid (CA), one of the most commonly occurring phenolic acids in fruits, grains and dietary supplements, was evaluated for its protective effect against the Ni induced oxidative damage in liver. In this investigation, Ni (20 mg/kg body weight) was administered intraperitoneally for 20 days to induce toxicity. CA was administered orally (15, 30 and 60 mg/kg body weight) for 20 days with intraperitoneal administration of Ni. Ni induced liver damage was clearly shown by the increased activities of serum hepatic enzymes namely aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), gamma glutamyl transferase (GGT) and lactate dehydrogenase (LDH) along with increased elevation of lipid peroxidation indices (thiobarbituric reactive acid substances (TBARS) and lipid hydroperoxides). The toxic effect of Ni was also indicated by significantly decreased levels of enzymatic (superoxide dismutase (SOD), catalase (CAT) glutathione peroxidase (GPx) and glutathione S-transferase (GST)) and non-enzymatic antioxidants (glutathione (GSH), vitamin C and vitamin E). CA administered at a dose of 60 mg/kg body weight significantly reversed the activities of hepatic marker enzymes to their near normal levels when compared with other two doses. In addition, CA significantly reduced lipid peroxidation and restored the levels of antioxidant defense in the liver. All these changes were supported by histological observations. The results indicate that CA may be beneficial in ameliorating the Ni induced oxidative damage in the liver of rats. SN - 0009-2797 UR - https://www.unboundmedicine.com/medline/citation/18405891/Efficacy_of_caffeic_acid_in_preventing_nickel_induced_oxidative_damage_in_liver_of_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0009-2797(08)00134-8 DB - PRIME DP - Unbound Medicine ER -