ツジ マユミ   Tsuji Mayumi
  辻 真弓
   所属   医学部医学科  基礎医学系 衛生学
   職種   教授
論文種別 原著
言語種別
査読の有無 査読あり
表題 Involvement of reactive oxygen species derived from mitochondria in neuronal injury elicited by methylmercury.
掲載誌名 正式名:Journal of clinical biochemistry and nutrition
略  称:J Clin Biochem Nutr
ISSNコード:09120009/09120009
巻・号・頁 59(3),182-190頁
著者・共著者 Ishihara Yasuhiro, Tsuji Mayumi, Kawamoto Toshihiro, Yamazaki Takeshi
発行年月 2016/11
概要 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 ρ(0) 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 ρ(0) cells. Our ρ(0) 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 ρ(0) cells, indicating that ρ(0) cells are resistant to methylmercury-induced oxidative stress. ρ(0) cells also showed tolerance against hydrogen peroxide and superoxide anion, suggesting that ρ(0) 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.
DOI 10.3164/jcbn.16-19
PMID 27895385