Rip1 enhances methyl mercury toxicity through production of reactive oxygen species (ROS) in budding yeast

Jin Yong Lee, Gi Wook Hwang, Akira Naganuma

研究成果: Article査読

5 被引用数 (Scopus)

抄録

Reactive oxygen species (ROS) produced by mitochondria are potentially involved in the manifestation of methylmercury toxicity. However, the molecular mechanism underlying methylmercury toxicity remains poorly understood. We examined susceptibility to methylmercury in yeast strains that each lacked one of components of the mitochondrial electron transport system. Resistance to methylmercury was exhibited only by yeast that lacked Rip1, a component of electron transport system complex III. Resistance to methylmercury in Rip1-deficient yeast was independent of the activity of electron transport system complex III. Also, ROS levels induced by methylmercury in Rip1-deficient yeast were significantly lower than in wild-type yeast. Thus, Rip1 is potentially involved in ROS production through an as-yet unknown mechanism that is independent of the activity of electron transport system complex III, thereby enhancing methylmercury toxicity.

本文言語English
ページ(範囲)715-717
ページ数3
ジャーナルJournal of Toxicological Sciences
34
6
DOI
出版ステータスPublished - 2009 12

ASJC Scopus subject areas

  • Toxicology

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