铁很重要:老化的微塑料破坏了肝脏器官中的铁平衡
Wei Cheng1, Yue Zhou1, Hange Chen1
1School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
The Science of the total environment
|October 3, 2023
概括
老化微塑料 (aMP) 显示出比原始微塑料 (pMP) 更大的肝毒性. 陈旧的聚乙烯微塑料破坏肝脏器官中的铁稳态和线粒体功能,突出显示微塑料暴露的潜在健康风险.
科学领域:
- 环境毒理学环境毒理学
- 细胞生物学 细胞生物学
- 材料科学 材料科学 材料科学
背景情况:
- 塑料产品通过日常使用降解为老化微塑料 (aMP).
- 人类接触到aMP,肝脏是关键的标器官.
- 有限的研究比较了aMP与原始微塑料 (pMP) 的肝毒性.
研究的目的:
- 为了比较老化聚烯微塑料 (aPS) 和原始聚烯微塑料 (pPS) 在人类肝脏器官 (LO) 中的细胞毒性.
- 调查aPS暴露对铁稳态,线粒体功能和LOs中的氧化应激的影响.
- 探索N-乙半氨酸 (NAC) 的潜在保护作用和铁过载 (铁氨基酸盐 - FAC) 对aPS诱导的肝毒性的恶化作用.
主要方法:
- 培养的人类多能干细胞衍生肝脏器官 (LO).
- 暴露于不同度的pPS和aPS (1微米) 的LOs.
- 分析了细胞毒性,铁含量 ([Fe2+],[Fe3+]),铁运输标记 (TFRC,SLC7A11,FTL,FTH1),线粒体形态,脂质过氧化和GSH过氧化酶活性.
- 使用FAC用于铁过载和NAC用于氧化应激调制.
主要成果:
- aPS在LOs中表现出比pPS更高的细胞毒性.
- aPS暴露破坏了铁的稳态,由改变的铁含量和与费里轻链 (FTL) 的同定位表明,这表明"矢量效应".
- 观察到异常的线粒体形态,增加脂质过氧化,减少GSH过氧化酶活性,以及铁相关基因 (TFRC,SLC7A11,FTL,FTH1) 的改变表达.
- 铁过载加剧了aPS的毒性,而NAC部分减轻了氧化应激,但没有完全逆转肝毒性.
- 低剂量的aMP (50 ng/mL) 诱导了FTL和FTH1表达的特定二态变化.
结论:
- 陈旧的微塑料比原始的微塑料对肝脏的风险更大.
- aPS诱导的肝毒性涉及铁平衡和线粒体功能障碍的破坏.
- 需要进一步的研究,以了解aMP暴露的长期健康影响及其在肝脏中的特定机制.
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