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来自中国一座特大城市的降尘微塑料通过PI3K/Akt/mTOR途径抑制自噬。

Dust Fall Microplastics from a Megacity of China Inhibit Autophagy via the PI3K/Akt/mTOR Pathway.

作者信息

Ma Yajing, Yu Jinjin, Sun Jian, Zhu Yuantong, Li Xuan, Liu Xinyao, Zhang Xinya, Liu Lingyi, Li Lingli, Yang Jiaer, Li Weifeng, Ho Kin-Fai, Shen Zhenxing, Niu Xiaofeng

机构信息

School of Pharmacy, Xi'an Jiaotong University, Xi'an 710061, China.

Department of Environmental Sciences and Engineering, Xi'an Jiaotong University, Xi'an, 710049, China.

出版信息

Environ Health (Wash). 2025 Jan 27;3(5):469-481. doi: 10.1021/envhealth.4c00200. eCollection 2025 May 16.

Abstract

The problem of microplastics (MPs) pollution has caused many health risks to residents of Chinese cities. In this study, nine kinds of MPs or microrubbers (MRs) from dust fall (DF) in Xi'an, a megacity in northwestern China, were measured by pyrolysis-gas chromatography-mass spectroscopy, namely, polyethylene, polypropylene, nylon 88, polybutylene, polytetrafluorethylene, polyisoprene, polyvinyl chloride, natural rubber, and synthesis rubber. Here, 51.20% of MPs were extracted from the original DF (samples denoted DF-O). After the subtracting procedure, MPs and their residual (DF-S samples) were divided into two parts. Our results indicated that the DF-O and MPs samples exhibited higher cytotoxicity, inflammatory, and oxidative stress levels than the DF-S samples did. The DF-O and MPs samples suppressed autophagy by decreasing expression levels of microtubule-associated protein light chain 3 (LC3B), p-phosphatidylinositol 3-kinase (p-PI3K), phosphorylated AKT protein (p-Akt), and p-mammalian target of rapamycin (p-mTOR) while increasing the level of p62. Meanwhile, DF-O and MPs samples induced apoptosis through increasing levels of Bax/Bcl-2 and Cleaved Caspase-3/Caspase-3 in Raw264.7 cells. These trends could be reversed through removing half of the MPs in DF-O. Therefore, dust fall microplastics inhibited autophagy and induced apoptosis via activating the PI3K/Akt/mTOR pathway, increasing the Bax/Bcl-2 and Cleaved Caspase-3/Caspase-3 ratios. Here we provide a comprehensive perspective into the studies of atmospheric MPs pollution status and mechanisms of inhalation toxicity for health risk assessment of MPs in DF.

摘要

微塑料(MPs)污染问题已给中国城市居民带来诸多健康风险。在本研究中,采用热解-气相色谱-质谱法对中国西北部大城市西安降尘(DF)中的9种微塑料或微橡胶(MRs)进行了测定,分别为聚乙烯、聚丙烯、尼龙88、聚丁烯、聚四氟乙烯、聚异戊二烯、聚氯乙烯、天然橡胶和合成橡胶。在此,51.20%的微塑料是从原始降尘(标记为DF-O的样品)中提取的。经过减除程序后,微塑料及其残留物(DF-S样品)被分为两部分。我们的结果表明,DF-O和微塑料样品的细胞毒性、炎症和氧化应激水平高于DF-S样品。DF-O和微塑料样品通过降低微管相关蛋白轻链3(LC3B)、磷酸化磷脂酰肌醇3激酶(p-PI3K)、磷酸化AKT蛋白(p-Akt)和磷酸化哺乳动物雷帕霉素靶蛋白(p-mTOR)的表达水平,同时增加p62水平来抑制自噬。同时,DF-O和微塑料样品通过提高Raw264.7细胞中Bax/Bcl-2和裂解型半胱天冬酶-3/半胱天冬酶-3的水平诱导细胞凋亡。通过去除DF-O中一半的微塑料,这些趋势可以逆转。因此,降尘微塑料通过激活PI3K/Akt/mTOR途径,增加Bax/Bcl-2和裂解型半胱天冬酶-3/半胱天冬酶-3的比例来抑制自噬并诱导细胞凋亡。在此,我们为大气微塑料污染状况及吸入毒性机制的研究提供了一个全面的视角,以评估降尘中微塑料的健康风险。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6346/12090011/e09628146c56/eh4c00200_0001.jpg

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