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聚乙烯纳米塑料通过以太脂积累引发了Nrf2缺乏肠道中的铁亡

Boxuan Liang¹, Xiyun Huang¹, Zhiming Li¹

¹National Medical Products Administration (NMPA) Key Laboratory for Safety Evaluation of Cosmetics, Guangdong Provincial Key Laboratory of Tropical Disease Research, Department of Toxicology, School of Public Health, Southern Medical University, Guangzhou 510515, China.

Environment international

|March 13, 2025

概括

环境纳米塑料 (NP) 在肠道中触发细胞死亡通路ferroptosis. Nrf2蛋白质可以防止这种损伤,但高脂肪饮食会加剧NP毒性,特别是在易受伤害的个体中.

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:

纳米塑料 (NP) 是无处不在的环境污染物,人们越来越担心它们对胃肠道健康的影响.
以前的研究将NP暴露与通过氧化应激引起的肠道毒性联系在一起,但具体的细胞死亡机制尚不清楚.

研究的目的:

研究肠道上皮细胞中由聚乙烯纳米塑料 (PS-NPs) 诱导的细胞死亡机制.
确定Nrf2的作用,一个关键的氧化应激调节器,在PS-NP诱导的肠道毒性.

主要方法:

肠上皮特异性Nrf2缺乏的小鼠和人类Caco-2细胞暴露于环境相关的PS-NP度.
对细胞死亡途径,脂质过氧化和以太脂代谢的分析.
评估高脂肪饮食对PS-NP毒性的影响.

主要成果:

在肠道上皮细胞中,PS-NPs诱导了脂质过氧化驱动的细胞死亡的一种形式 - - 铁亡.
Nrf2缺乏症加剧了PS-NP诱导的铁亡.
暴露于PS-NP干扰了以太脂代谢,增加了脂质过氧化和铁灭症的易感性.
高脂肪饮食加剧了这些影响.

结论:

Nrf2在肠道中扮演着对PS-NP诱导的铁亡的关键保护作用.
质脂代谢的破坏是PS-NP毒性的关键机制.
减少Nrf2活性和不良饮食习惯的个人特别容易受到环境PS-NP暴露.

关键词:

新出现的污染物新出现的污染物表皮特异性的Nrf2缺乏症质脂以太是一种脂.铁化是铁化的一种.脂质代谢脂质代谢是一种

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