伊普可纳会诱导SH-SY5Y细胞中的氧化应激,细胞死亡和炎症
Carlos Villaorduña1, Mariano Mendoza-Carlos2, Manuel Chuyma2
1Faculty of Pharmacy, Universidad Nacional Mayor de San Marcos, Lima 15021, Peru.
Toxics
|July 28, 2023
概括
抗真菌杀虫剂伊普科纳 (ipconazole) 通过降低细胞活力和增加人类神经母细胞瘤细胞中的氧化应激,导致神经毒性. 这种农药暴露可能导致神经退行,凸显了环境健康问题.
科学领域:
- 环境毒理学环境毒理学
- 神经科学是一个神经科学.
- 细胞生物学 细胞生物学
背景情况:
- 伊普科纳是一种广泛使用的抗真菌农业化学品.
- 它的环境积累对人类和动物健康构成风险.
- 伊普科纳的神经毒性作用需要进行彻底的研究.
研究的目的:
- 研究伊普康纳对SH-SY5Y神经母细胞瘤细胞的细胞毒性作用.
- 为了阐明背后的分子机制ipconazole诱导的神经毒性.
- 评估伊普科纳对细胞死亡,氧化应激,炎症和抗氧化途径的影响.
主要方法:
- SH-SY5Y细胞在24小时内暴露在不同度的ipconazole (1-100μM) 中.
- 使用MTT试验评估了细胞活力.
- 分析了ROS的产生,酶3/7活性和基因表达 (Bax, Casp3, APAF1, BNIP3, Bcl2, NLRP3, Casp1, IL1β, NFκB, TNFα, IL6, NRF2, SOD, GPx) 的情况.
主要成果:
- 可纳显著降低了细胞活力,IC50为32.3μM.
- 可纳增加了反应性氧物种 (ROS) 生产和卡斯帕酶3/7活性.
- 可纳诱导细胞死亡,炎症和炎症基因的过度表达,同时降低抗氧化基因的调节.
结论:
- 伊普可纳在SH-SY5Y细胞中表现出剂量依赖的细胞毒性.
- 杀虫剂通过氧化应激和亡诱导神经毒性.
- 暴露于ipconazole是神经退行症的潜在危险因素.
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