通过PMK-1介导途径对神经毒性的PFOS和OBS的明显影响
Jiahong Jiang1, Qi Liu1, Boxiang Zhang1
1Institute of Environmental Systems Biology, College of Environment Science and Engineering, Dalian Maritime University, Linghai Road 1, Dalian 116026, China.
Toxics
|August 27, 2025
概括
在C. elegans中,p- perfluorous nonenoxybenzenesulfonate (OBS) 比 perfluorooctanesulfonic acid (PFOS) 更具有神经毒性,通过PMK-1途径影响神经元功能和行为.
科学领域:
- 环境科学
- 毒理学
- 神经科学
背景情况:
- p-非硫酸盐 (OBS) 是一种被提议的甲硫酸 (PFOS) 的替代品.
- 有关OBS的环境持久性和潜在毒性令人担忧.
- OBS的神经毒性机制尚不清楚.
研究的目的:
- 研究和比较OBS和PFOS的神经毒性作用和机制.
- 阐明PMK-1途径在OBS诱导的神经毒性的作用.
主要方法:
- 在24小时内暴露于OBS (0.1-100μM) 或PFOS (100μM) 的C. elegans.
- 神经行为分析,包括喉抽,头部摆动和身体曲.
- 测量神经元光强度和神经递质相关的基因表达.
- 对活性氧物种 (ROS) 生产和抗氧化基因表达的评估.
- 分子对接以确定与PMK-1的结合亲和力.
- 进行pmk-1基因突变分析.
主要成果:
- OBS 诱导了度依赖的神经行为缺陷,超过了 PFOS 在 100 μM 的效果.
- OBS和PFOS都降低了神经元光,降低了神经递质基因,增加了ROS,并抑制了抗氧化基因表达.
- 与PFOS相比,OBS对PMK-1的结合亲和力更强.
- OBS和PFOS上调了pmk-1和skn-1.
- pmk-1突变差异性影响了OBS诱导的神经毒性.
结论:
- 在C. elegans中,OBS表现出比PFOS更强的神经毒性.
- 通过PMK-1途径调解OBS诱导的神经毒性.
- OBS 需要进一步的安全研究作为 PFOS 的替代品.
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