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伊米达克洛普里德通过线粒体功能障碍和氧化应激影响人类细胞
Fenghua Wei1, Fei Cheng2, Huizhen Li3
1School of Chemistry and Environment, Jiaying University, Meizhou 514015, China; Guangdong Provincial Key Laboratory of Environmental Pollution and Health, College of Environment and Climate, Jinan University, Guangzhou 510632, China.
The Science of the total environment
|August 11, 2024
概括
尼奥尼科丁类杀虫剂伊米达克洛普里德破坏人类细胞线粒体,导致氧化应激,DNA损伤和亡. 这突出了超出神经毒性的潜在人类健康风险,强调了线粒体毒性问题.
科学领域:
- 环境毒理学环境毒理学
- 细胞毒理学 细胞毒理学
- 人类健康风险评估评估 人类健康风险评估
背景情况:
- 全球范围内广泛使用的尼奥尼科丁类杀虫剂.
- 有关超出神经毒性的非标生物毒性存在担忧.
- 通过额外的毒性途径出现潜在的人类健康风险.
研究的目的:
- 研究伊米达克洛普里德对人类神经母细胞瘤SH-SY5Y细胞的影响.
- 检查线粒体功能,氧化应激,DNA损伤和基因转录.
- 评估与伊米达克洛普里德暴露相关的潜在人类健康风险.
主要方法:
- 在48小时内,将SH-SY5Y细胞暴露在不同度的伊米达克洛普里德 (0.05200μmol/L) 中.
- 测定线粒体功能,包括腺三酸盐 (ATP) 和线粒体膜潜力 (MMP).
- 测量反应性氧物种 (ROS),过氧化 (H2O2),离子水平,DNA损伤和基因转录.
主要成果:
- 伊米达克洛普里德诱导了线粒体功能障碍,降低了ATP和MMP水平.
- 观察到氧化应激,随着ROS和H2O2生成的增加.
- 在高于47.6μmol/L的度下,发生了DNA损伤和亡.
- ATP 降解是最敏感的终点 (EC50 = 0.74 μmol/L).
结论:
- 伊米达克洛普里德暴露导致线粒体功能障碍和氧化应激在人类神经母细胞瘤细胞.
- 这些影响可能导致DNA损伤和亡,表明潜在的人类健康风险.
- 这项研究支持进一步研究人类内尼古丁类药物诱导的线粒体毒性.
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