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

Jin Yong Lee, Gi Wook Hwang, Akira Naganuma

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)715-717
Number of pages3
JournalJournal of Toxicological Sciences
Volume34
Issue number6
DOIs
Publication statusPublished - 2009 Dec

Keywords

  • Methylmercury
  • ROS
  • Resistance
  • Rip1
  • Yeast

ASJC Scopus subject areas

  • Toxicology

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