Contribution of Xanthine Oxidase-Derived Oxygen Free Radicals to the Development of Carbon Tetrachloride-Induced Acute Liver Injury in Rats

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We examined how oxygen free radicals derived from xanthine oxidase (XOD) contribute to the development of carbon tetrachloride (CCl4)-induced acute liver injury in rats. In rats treated with CCl4 (1ml/kg), liver injury appeared 3h after the treatment and developed by 24h, judged from the serum levels of transaminases. Hepatic and serum XOD activities and serum uric acid concentration did not change 6h after CCl4 treatment, but they all increased at 12h and further increased at 24h. An increase in the concentration of thiobarbituric acid reactive substances (TBARS), an index of lipid peroxidation, and decreases in reduced glutathione concentration and Cu, Zn-superoxide dismutase (SOD) activity, but not Mn-SOD activity, were observed in the liver at 6h after CCl4 treatment and these changes were further enhanced at 24h. When allopurinol (50mg/kg), an XOD inhibitor, was administered to CCl4-treated rats 6h after CCl4 treatment, liver injury progression was prevented with attenuation of increased hepatic and serum XOD activities, serum uric acid concentration, and hepatic TBARS concentration and decreased hepatic reduced glutathione concentration and Cu, Zn-SOD activity at 24h after CCl4 treatment. These results indicate that XOD-derived oxygen free radicals contribute to the progression of CCl4-induced acute liver injury in rats both by stimulating hepatic lipid peroxidation and by disrupting hepatic antioxidant defense system.

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詳細情報 詳細情報について

  • CRID
    1390282679649008512
  • NII論文ID
    130003670583
  • DOI
    10.3164/jcbn.33.83
  • COI
    1:CAS:528:DC%2BD2cXjtFGkt7c%3D
  • ISSN
    18805086
    09120009
    http://id.crossref.org/issn/09120009
  • Web Site
    https://search.jamas.or.jp/link/ui/2005139540
  • 本文言語コード
    en
  • データソース種別
    • JaLC
    • Crossref
    • CiNii Articles
  • 抄録ライセンスフラグ
    使用不可

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