Tryptophan metabolism in acute hepatic failure-induced mice.

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  • Mizoguchi Yasuhiro
    The Third Department of Internal Medicine, Osaka City University Medical School
  • Sakagami Yoshihide
    The Third Department of Internal Medicine, Osaka City University Medical School
  • Seki Shuichi
    The Third Department of Internal Medicine, Osaka City University Medical School
  • Kobayashi Kenzo
    The Third Department of Internal Medicine, Osaka City University Medical School
  • Yamamoto Sukeo
    The Osaka Socio-Medical Center Hospital
  • Morisawa Seiji
    The First Department of Biochemistry, Osaka City University Medical School

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  • 免疫学的急性肝不全誘導マウスにおけるトリプトファン代謝について

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Abstract

Massive hepatic cell necrosis can be induced in mice by an intravenous injection of Propionibacterium acnes (P. acnes) followed by an intravenous injection of a small mount of lipopolysaccharide (LPS) 7 days later. Using this experimentally-induced acute hepatic failure model, the products of tryptophan (TRP) metabolism during hepatocytotoxicity were studied. As a result, in acute hepatic failure-induced mice, blood indoleacetic acid (IAA) level increased before the increase in serum transaminase level, and its peak was seen 21 hours before that of transaminase. In addition, when hepatic cells separated from the mice were loaded with TRP and cultured with the cytotoxic factor produced from activated liver adherent cells, IAA level of the hepatic cells increased remarkably.<br>These results suggest that during hepatocytotoxicity, the change from kynurenine to nicotinamide by the major pathway of TRP metabolism may be inhibited, and that the pathway from TRP to tryptamine to IAA may be impaired.

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