线粒体综合体I的过度活化导致PET微塑料诱导的肠道生物能量崩.
Chuxin Zhang1, Wenjing Li2, Jiaxing An1
1School of Forensic Medicine, Shanxi Medical University, Shanxi Key Laboratory of Forensic Medicine, and Key Laboratory of Forensic Toxicology, Ministry of Public Security, Jinzhong 030600, China.
Journal of hazardous materials
|February 3, 2026
概括
聚乙烯二甲 (PET) 微塑料 (MP) 的消化变化导致肠道功能障碍和代谢毒性. 这些改变的MP破坏葡萄糖代谢和线粒体功能,导致氧化应激和饮食暴露的潜在健康风险.
科学领域:
- 环境科学 环境科学
- 毒理学 毒理学 毒理学
- 生物化学 生物化学
背景情况:
- 聚乙烯二甲 (PET) 微塑料 (MPs) 是广泛存在的环境污染物,人类已知暴露途径.
- 摄入的MPs可以穿过肠道屏障,进入血液循环,并在器官中积累,造成潜在的健康风险.
研究的目的:
- 为了研究消化转化对PETMPs的影响.
- 阐明消化的PETMPs诱导肠道功能障碍和代谢毒性的机制.
主要方法:
- 从商业瓶子和模拟胃肠道中利用了生理上相关的PET MP.
- 采用高分辨率呼吸计和集成的多omics分析.
- 评估了对葡萄糖运输 (GLUT2),糖解,线粒体呼吸,氧化应激标志物 (ROS,脂质过氧化) 和ATP合成的影响.
主要成果:
- 消化后的PETMPs抑制GLUT2,导致葡萄糖积累和糖解阻塞.
- 线粒体综合体I显示功能障碍的过活化,导致ROS生成增加和ATP合成关闭.
- 观察到显著的氧化应激,脂质过氧化和线粒体生物能学受损,表明代谢崩.
结论:
- 消化转化PETMPs作为代谢毒性的强有力的驱动因素.
- 发现了一种涉及线粒体功能障碍和氧化应激的新型毒性机制.
- 这些发现为评估与饮食中的微塑料暴露相关的健康风险提供了一个机制框架.
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