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- Tokumoto Maki
- Laboratory of Pharmaceutical Health Sciences, School of Pharmacy, Aichi Gakuin University
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- Shibuya Kiyoshi
- Department of Pharmacy, Kitasato University Medical Center
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- Lee Jin-Yong
- Laboratory of Pharmaceutical Health Sciences, School of Pharmacy, Aichi Gakuin University
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- Tohyama Chiharu
- Faculty of Medicine, University of Tsukuba National Institute for Environmental Studies
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- Satoh Masahiko
- Laboratory of Pharmaceutical Health Sciences, School of Pharmacy, Aichi Gakuin University National Institute for Environmental Studies
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抄録
<p>Metallothionein (MT) is a small, metal-binding protein that can act as a scavenger of free radicals. To determine whether MT is involved in ethanol-induced hepatotoxicity, which is known to occur through oxidative stress, we studied sensitivity to hepatotoxicity caused by ethanol in MT-null mice genetically deleted for MT-I and MT-II. MT-null mice and wild-type mice were i.p. administrated with ethanol (99.5%, 2.0 g/kg). The increase in GPT, GOT, and LDH activities in the serum of MT-null mice was significantly higher than in the wild-type mice 24 hr after ethanol treatment. Histopathological examination in the liver of ethanol-treated MT-null mice demonstrated vacuolar degeneration. In contrast, histopathologic change was less prominent in the liver of ethanol-treated wild-type mice. Moreover, ethanol increased lipid peroxidation levels only in the liver of MT-null mice. These results indicate that deletion of MT is associated with ethanol-induced severe hepatotoxicity through oxidative stress.</p>
収録刊行物
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- Fundamental Toxicological Sciences
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Fundamental Toxicological Sciences 4 (6), 269-273, 2017
一般社団法人 日本毒性学会
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詳細情報 詳細情報について
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- CRID
- 1390001205764898048
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- NII論文ID
- 130006250779
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- ISSN
- 2189115X
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- Crossref
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可