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Measurements of Physiological Stress Responses in C. Elegans
Published on: May 21, 2020
Rip1 enhances methylmercury toxicity through production of reactive oxygen species (ROS) in budding yeast
Jin-Yong Lee1, Gi-Wook Hwang, Akira Naganuma
1Laboratory of Molecular and Biochemical Toxicology, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Miyagi, Japan.
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.
Insights
Mitochondrial reactive oxygen species (ROS) contribute to methylmercury toxicity. Yeast lacking Rip1 showed resistance, indicating Rip1
Area of Science:
- Biochemistry
- Toxicology
- Cell Biology
Background:
- Mitochondria generate reactive oxygen species (ROS) implicated in methylmercury toxicity.
- The precise molecular mechanisms of methylmercury toxicity are not fully understood.
Purpose of the Study:
- To investigate the role of mitochondrial components in methylmercury susceptibility.
- To elucidate the molecular pathways of methylmercury toxicity.
Main Methods:
- Utilized yeast strains deficient in specific mitochondrial electron transport system (ETS) components.
- Assessed methylmercury resistance and ROS production in wild-type versus knockout yeast strains.
Main Results:
- Only yeast lacking Rip1 (a component of ETS complex III) exhibited resistance to methylmercury.
- This resistance was independent of ETS complex III activity.
- Rip1-deficient yeast showed significantly lower ROS levels when exposed to methylmercury compared to wild-type.
Conclusions:
- Rip1 plays a crucial role in methylmercury-induced ROS production via an unknown mechanism.
- This Rip1-mediated ROS production enhances methylmercury toxicity.
- Targeting Rip1 may offer a novel strategy for mitigating methylmercury toxicity.
