通过食物传播的PET微塑料污染通过线粒体-AMPK-DNA损伤途径破坏肠道屏障
Chuxin Zhang1, Yitao Yan2, Xu Li1
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 agricultural and food chemistry
|February 9, 2026
概括
聚乙烯二甲) 微塑料 (PET-MPs) 通过破坏线粒体,激活AMPK,并诱导DNA断裂,导致肠道损伤. 抑制AMPK可以减轻这些有害影响,揭示了微塑料毒性的关键途径.
科学领域:
- 环境健康 环境健康
- 毒理学 毒理学 毒理学
- 细胞生物学 细胞生物学
背景情况:
- 聚乙烯二甲) 微塑料 (PET-MPs) 是常见的饮食污染物.
- 人体肠道中PET-MP毒性背后的机制尚不清楚.
研究的目的:
- 研究消化肠道中消化的PET-MPs对人类肠道上皮细胞的毒性.
- 为了阐明PET-MP诱导的肠损伤的分子机制.
主要方法:
- 使用了人类肠道上皮细胞培养模型,暴露在消化的PET-MPs中24小时.
- 进行非目标代谢,以确定受干扰的细胞通路.
- 进行功能验证测试,包括线粒体功能测试和DNA损伤评估.
- 研究了AMPK信号通路及其抑制的作用.
主要成果:
- 消化的PET-MPs诱导了细胞毒性,氧化应激,屏障破坏和细胞因子失调.
- 代谢学发现AMPK信号通路是关键受影响的节点.
- PET-MPs导致线粒体损伤,导致ATP耗尽和随后的AMPK激活.
- 激活AMPK介导的细胞增殖停止和DNA双链断裂.
- 药理上抑制AMPK可以减少屏障缺陷和DNA损伤.
结论:
- 一个新的线粒体功能障碍-AMPK激活-DNA损伤轴被确定为PET-MP诱导的肠损伤的中心机制.
- 这些发现为与微塑料暴露相关的健康风险提供了关键的机制性见解.
- 向AMPK途径可能提供一种治疗策略,以减轻微塑料诱导的肠道损伤.
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