双S通过血管内皮细胞中的线粒体通路诱导内皮功能障碍,以及结合专蛋白的排毒效应
Rong Tian1, Jia-Xin Li1, Naihao Lu1
1College of Chemistry and Materials, Key Laboratory of Green Catalysis of Jiangxi Education Institutes, Jiangxi Normal University, Nanchang, 330022, China.
Chemico-biological interactions
|January 10, 2025
概括
双S (BPS) 是一种BPA的替代物,通过增加线粒体的活性氧物种 (ROS) 来引起内皮功能障碍. 结合白蛋白减轻了这些有害影响,表明对BPS毒性有保护作用.
科学领域:
- 环境健康 环境健康
- 毒理学 毒理学 毒理学
- 心血管研究研究心血管研究
背景情况:
- 双S (BPS) 是消费品中双A (BPA) 的常见替代品.
- 流行病学研究将BPS暴露与血管疾病联系起来,但其生物机制尚不清楚.
研究的目的:
- 研究BPS对内皮功能及其潜在机制的影响.
- 探索白蛋白对BPS毒性的潜在保护作用.
主要方法:
- 用人静脉内皮细胞 (HUVEC) 和小鼠动脉来评估BPS的影响.
- 测量了线粒体功能,氧化 (NO) 形成和反应性氧物种 (ROS) 生产.
- 使用生物物理方法分析了白蛋白-BPS相互作用.
主要成果:
- 在HUVEC中,BPS暴露剂量依赖于内皮功能受损,减少NO的形成,增加ROS和线粒体功能障碍.
- 线粒体ROS调解BPS诱导的内皮功能障碍,SOD被确定为敏感的目标.
- 在小鼠中,饮食中的BPS暴露损害了NO的形成和血管扩张.
- 牛血清白蛋白 (BSA) 与BPS结合显著降低了ROS和受保护的内皮细胞.
结论:
- 饮食中的BPS暴露通过诱导线粒体ROS和内皮功能障碍来破坏血管平衡.
- 专蛋白对抗BPS的危险影响,具有显著的排毒作用.
- 了解BPS毒性机制对于公共卫生和环境安全至关重要.
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