氧化应激作为2,6-二-1,4-基诱导的神经发育毒性的关键事件
Ting Liu1, Xin Chen2, Wanling Li3
1School of Public Health, Jilin University, Changchun, Jilin 130021, China; The First Hospital, Jilin University, Changchun, Jilin 130021, China.
Ecotoxicology and environmental safety
|August 20, 2023
概括
2,6-二-1,4-基 (DCBQ) 是饮用水消毒的副产品,通过诱导神经细胞中的氧化应激和亡,导致神经发育毒性. 像NAC这样的抗氧化剂可以减轻这些有害影响.
科学领域:
- 环境科学 环境科学
- 毒理学 毒理学 毒理学
- 神经科学是一个神经科学.
背景情况:
- 2,6-二-1,4-基 (DCBQ) 是饮用水中的新出现的污染物.
- 像DCBQ这样的消毒副产品 (DBPs) 具有潜在的健康风险.
- 关于DCBQ对神经发育的影响的全面毒理学数据有限.
研究的目的:
- 使用体外模型研究DCBQ的神经发育毒性.
- 阐明DCBQ诱导的神经毒性背后的机制.
- 评估抗氧化剂对DCBQ神经毒性的保护作用.
主要方法:
- 利用神经分化SH-SY5Y细胞作为一个体外模型.
- 评估了细胞活力,神经分化,活性氧物种 (ROS) 生成,亡和线粒体膜潜力.
- 研究了氧化应激和信号通路 (PI3K/AKT/mTOR) 在DCBQ毒性的作用.
- 评估了N-乙-L-氨酸 (NAC) 作为潜在的抗氧化治疗的疗效.
主要成果:
- 暴露于DCBQ显著降低了细胞活力和神经分化.
- DCBQ增加了ROS水平,细胞亡,并降低了线粒体膜潜力.
- DCBQ诱导的神经毒性与氧化应激和线粒体亡途径的激活有关.
- NAC治疗减轻了DCBQ诱导的神经毒性影响,这表明氧化应激有作用.
- DCBQ 抑制了 PI3K/AKT/mTOR 的生存途径.
结论:
- 在实验室中DCBQ表现出显著的神经发育毒性.
- 氧化应激和线粒体功能障碍是DCBQ神经毒性的关键机制.
- 暴露于DCBQ会影响神经细胞的增殖和生存.
- 这些发现强调了评估DBP如DCBQ的神经发育风险的重要性.
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