Rip1 enhances methylmercury toxicity through production of reactive oxygen species (ROS) in budding yeast.
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.
Lee
Jin-Yong
JY
Laboratory of Molecular and Biochemical Toxicology, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Miyagi, Japan.
Hwang
Gi-Wook
GW
Naganuma
Akira
A
D002478:Cells, Cultured; D004579:Electron Transport; D014450:Electron Transport Complex III / Q000502:physiology; D008767:Methylmercury Compounds / Q000633:toxicity*; D008928:Mitochondria / Q000378:metabolism; D028861:Nuclear Pore Complex Proteins / Q000502:physiology*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D029701:Saccharomyces cerevisiae Proteins / Q000502:physiology*; D004718:Saccharomycetales / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism*
D008767:Methylmercury Compounds; C109212:NUP42 protein, S cerevisiae; D028861:Nuclear Pore Complex Proteins; D017382:Reactive Oxygen Species; D029701:Saccharomyces cerevisiae Proteins; D014450:Electron Transport Complex III