Metallothionein-Null Mice Are Sensitive to Endotoxine/D-Galactosamine-Induced Hepatotoxicity.

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  • Kimura Tomoki
    Department of Toxicology, Graduate School of Pharmaceutical Sciences, Osaka University
  • Koujitani Takatoshi
    Department of Toxicology and Teratology, Developmental Research Laboratories, Dainippon Pharmaceutical Co., Ltd.
  • Itoh Norio
    Department of Toxicology, Graduate School of Pharmaceutical Sciences, Osaka University
  • Takehara Miyako
    Department of Toxicology, Graduate School of Pharmaceutical Sciences, Osaka University
  • Oguro Ikuyo
    Department of Toxicology, Graduate School of Pharmaceutical Sciences, Osaka University
  • Ishizaki Jun-ichi
    Department of Toxicology, Graduate School of Pharmaceutical Sciences, Osaka University
  • Nakanishi Tsuyoshi
    Department of Toxicology, Graduate School of Pharmaceutical Sciences, Osaka University
  • Tanaka Keiichi
    Department of Toxicology, Graduate School of Pharmaceutical Sciences, Osaka University

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  • Metallothionein-Null Mice Are Sensitive to Endotoxine/D-Galactosamine-Induced Hepatoxicity

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Metallothionein (MT), which is a low-molecular weight, cysteine-rich, metal-binding protein, is induced during acute-phase reactions. However, the specific function of MT in the acute-phase response remains to be elucidated. We previously reported that MT-I, II deficient (MT-null) mice are highly sensitive to the lethal effects of lipopolysaccharide (LPS)/D-galactosamine (GalN). We designed the present study to clarify the major cause of the differences in the sensitivity to the lethal effects of LPS/GalN between wild type and MT-null mice. We found that histological grade of hepatocellular necrosis, induced by LPS/GalN, was greater in MT-null mice than in wild type mice. Therefore, the present findings suggest that MT induction has the potential as an attenuator of LPS/GalN-induced liver necrosis

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