期刊
CELLS
卷 10, 期 4, 页码 -出版社
MDPI
DOI: 10.3390/cells10040888
关键词
LiPF6; genome-wide screen; mitochondrial damage; ROS; ATP content; oxidative phosphorylation
类别
资金
- Zhejiang Provincial Natural Science Foundation of China [LQ19C070001]
- National Natural Science Foundation of China [31800163]
- Swedish Cancer Fund (Cancerfonden) [CAN 2017/643, 19 0069]
- Swedish Natural Research Council (Vetenskapsradet) [VR 2015-04984, VR 2019-03604]
- Vinnova [2019-03604] Funding Source: Vinnova
- Swedish Research Council [2019-03604] Funding Source: Swedish Research Council
Research reveals that lithium hexafluorophosphate (LiPF6) is more toxic to yeast than lithium chloride or sodium hexafluorophosphate, causing mitochondrial damage, reactive oxygen species accumulation, and ATP content changes leading to cytotoxicity. Genome-wide screening shows oxidative phosphorylation-related gene deletion mutants are specifically hypersensitive to LiPF6, with higher ROS production and reduced ATP levels upon treatment, suggesting their importance in counteracting LiPF6-induced toxicity.
Lithium hexafluorophosphate (LiPF6) is one of the leading electrolytes in lithium-ion batteries, and its usage has increased tremendously in the past few years. Little is known, however, about its potential environmental and biological impacts. In order to improve our understanding of the cytotoxicity of LiPF6 and the specific cellular response mechanisms to it, we performed a genome-wide screen using a yeast (Saccharomyces cerevisiae) deletion mutant collection and identified 75 gene deletion mutants that showed LiPF6 sensitivity. Among these, genes associated with mitochondria showed the most enrichment. We also found that LiPF6 is more toxic to yeast than lithium chloride (LiCl) or sodium hexafluorophosphate (NaPF6). Physiological analysis showed that a high concentration of LiPF6 caused mitochondrial damage, reactive oxygen species (ROS) accumulation, and ATP content changes. Compared with the results of previous genome-wide screening for LiCl-sensitive mutants, we found that oxidative phosphorylation-related mutants were specifically hypersensitive to LiPF6. In these deletion mutants, LiPF6 treatment resulted in higher ROS production and reduced ATP levels, suggesting that oxidative phosphorylation-related genes were important for counteracting LiPF6-induced toxicity. Taken together, our results identified genes specifically involved in LiPF6-modulated toxicity, and demonstrated that oxidative stress and ATP imbalance maybe the driving factors in governing LiPF6-induced toxicity.
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