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Arachidonate metabolism in D-galactosamine or carbon tetrachloride-induced acute and chronic liver injuries in rats

  • Liver, Pancreas, and Biliary Tract
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Summary

Arachidonate metabolism was examined in rats with experimentally induced acute and chronic liver injuries. Acute liver injury was induced by a single administration of D-galactosamine (D-Galn) and lipopolysaccharide (LPS) or carbon tetrachloride (CCl4). Chronic liver injury was produced by several administrations of CCl4 for 5 weeks. Non-parenchymal liver cells from rats with D-Galn/LPS-induced acute liver injury produced prominantly leukotriene B4 and 5-hydroxy-arachidonic acid which were hardly synthesized by the normal rat liver. No apparent changes were observed in the arachidonate metabolism of the non-parenchymal cells of the acute CCl4-injured liver. In chronic liver injury, the production of 6-ketoprostaglandin F1α, a stable metabolite of prostaglandin I2, by the non-parenchymal cell fraction was significantly enhanced in contrast with the fixed amount of the other arachidonate metabolites. These results suggested the arachidonate metabolism by non-parenchymal liver cells might change according to the pathogenesis of the liver disease.

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Authors and Affiliations

  1. First Department of Biochemistry, Osaka City University Medical School, Osaka, Japan

    Ping Liu & Seiji Morisawa

  2. The Third Department of Internal Medicine, Osaka City University Medical School, 1-5-7 Asahi-machi, Abeno-ku, 545, Osaka, Japan

    Norifumi Kawada & Yasuhiro Mizoguchi M.D.

Authors
  1. Ping Liu
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  2. Norifumi Kawada
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  3. Yasuhiro Mizoguchi M.D.
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  4. Seiji Morisawa
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Liu, P., Kawada, N., Mizoguchi, Y. et al. Arachidonate metabolism in D-galactosamine or carbon tetrachloride-induced acute and chronic liver injuries in rats. Gastroenterol Jpn 27, 624–631 (1992). https://doi.org/10.1007/BF02774977

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  • DOI: https://doi.org/10.1007/BF02774977

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