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暴露于BPA激活了雌激素受体α (ER-α) 和ROS,以诱导耳毛细胞中的热亡
Jie Tang1, Bairu Chen2, Fang Yu1
1Department of Pathology, Provincial and Municipal Construction Discipline of Experimental Diagnostics, Jiaxing Hospital of Traditional Chinese Medicine, Jiaxing University, Jiaxing 314001, China.
Ecotoxicology and environmental safety
|September 23, 2025
概括
双甲 (BPA) 暴露会通过激活雌激素受体α (ER-α) 和触发线粒体反应性氧物种 (ROS) 来引起小鼠耳毛细胞的耳毒性,从而导致热致死. 抑制ROS或ER-α可以防止BPA诱导的细胞死亡.
科学领域:
- 环境毒理学环境毒理学
- 耳毒性研究研究 耳毒性研究
- 分子生物学分子生物学
背景情况:
- 环境污染物,包括双A (BPA),越来越多地与听力损失有关.
- BPA在耳毛细胞中诱导耳毒性的确切机制尚不清楚.
- 雌激素受体α (ER-α) 参与细胞对环境暴露的反应.
研究的目的:
- 在小鼠耳毛细胞中研究BPA诱导的耳毒性背后的分子机制 (HEI-OC1).
- 确定参与BPA介导的耳损伤的关键途径和分子点.
- 探索雌激素受体α (ER-α) 和活性氧物种 (ROS) 在 BPA 耳毒性中的作用.
主要方法:
- HEI-OC1细胞对不同度的BPA的剂量依赖性暴露.
- RNA转录组测序以识别差异表达的基因和途径.
- 分析细胞活力,活性氧物种 (ROS),线粒体膜潜力和热的标志物.
- 使用ROS清除剂N-乙半氨酸 (NAC) 和ER-α对抗剂富尔韦斯特兰特的抑制研究.
主要成果:
- 50微米以上的BPA度以剂量依赖的方式降低了细胞活力.
- RNA测序揭示了基因表达的显著变化,特别是雌激素受体相关基因的丰富和ER-α的上调.
- 暴露于BPA引起了类似于火灭的变化,增加了ROS和水平,并改变了线粒体功能.
- 抑制ROS或ER-α显著缓解了BPA诱导的细胞死亡和热.
结论:
- 通过一种涉及ER-α激活和线粒体ROS生成的机制,BPA暴露会诱导耳毛细胞的耳毒性.
- 这些通路在对BPA的反应中促进了 pyroptosis,一种被编程的细胞死亡形式.
- 准ER-α和ROS可能为缓解BPA引起的听力损失提供治疗策略.
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