Involvement of reactive oxygen species derived from mitochondria in neuronal injury elicited by methylmercury
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- Ishihara Yasuhiro
- Laboratory of Molecular Brain Science, Graduate School of Integrated Arts and Sciences, Hiroshima University
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- Tsuji Mayumi
- Department of Environmental Health, University of Occupational and Environmental Health
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- Kawamoto Toshihiro
- Department of Environmental Health, University of Occupational and Environmental Health
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- Yamazaki Takeshi
- Laboratory of Molecular Brain Science, Graduate School of Integrated Arts and Sciences, Hiroshima University
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<p>Methylmercury induces oxidative stress and subsequent neuronal injury. However, the mechanism by which methylmercury elicits reactive oxygen species (ROS) production remains under debate. In this study, we investigated the involvement of mitochondrial ROS in methylmercury-induced neuronal cell injury using human neuroblastoma SH-SY5Y-derived ρ0 cells, which have a deletion of mitochondrial DNA and thus decreased respiratory activity. SH-SY5Y cells were cultured for 60 days in the presence of ethidium bromide to produce ρ0 cells. Our ρ0 cells showed decreases in the cytochrome c oxidase expression and activity as well as oxygen consumption compared with original SH-SY5Y cells. Methylmercury at a concentration of 1 µM induced cell death with oxidative stress in original SH-SY5Y cells, but not ρ0 cells, indicating that ρ0 cells are resistant to methylmercury-induced oxidative stress. ρ0 cells also showed tolerance against hydrogen peroxide and superoxide anion, suggesting that ρ0 cells are resistant to total ROS. These data indicate that mitochondrial ROS are clearly involved in oxidative stress and subsequent cell death induced by methylmercury. Considering that the dominant mechanism of ROS generation elicited by methylmercury is due to direct antioxidant enzyme inhibition, mitochondria might play a role in amplifying ROS in methylmercury-induced neurotoxicity.</p>
収録刊行物
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- Journal of Clinical Biochemistry and Nutrition
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Journal of Clinical Biochemistry and Nutrition 59 (3), 182-190, 2016
一般社団法人 日本酸化ストレス学会
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詳細情報 詳細情報について
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- CRID
- 1390282679650511744
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- NII論文ID
- 130005268734
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- ISSN
- 18805086
- 09120009
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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
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- CiNii Articles
- KAKEN
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- 抄録ライセンスフラグ
- 使用不可