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大气细颗粒物(PM)和准超细微粒(PM)化学组分的毒理学评价。在人支气管上皮 BEAS-2B 细胞中的应用。

Toxicological appraisal of the chemical fractions of ambient fine (PM) and quasi-ultrafine (PM) particles in human bronchial epithelial BEAS-2B cells.

机构信息

Unité de Chimie Environnementale et Interactions sur le Vivant, UCEIV-EA 4492, FR CNRS, 3417, Univ. Littoral Côte d'Opale, Dunkerque, France; CHU Lille, Institut Pasteur de Lille, ULR 4483-IMPacts de l'Environnement Chimique sur la Santé (IMPECS), Univ. Lille, Lille, France; Lebanese Atomic Energy Commission, NCSR, Beirut, Lebanon.

Unité de Chimie Environnementale et Interactions sur le Vivant, UCEIV-EA 4492, FR CNRS, 3417, Univ. Littoral Côte d'Opale, Dunkerque, France.

出版信息

Environ Pollut. 2020 Aug;263(Pt A):114620. doi: 10.1016/j.envpol.2020.114620. Epub 2020 Apr 18.

Abstract

New toxicological research is still urgently needed to improve the current knowledge about the induction of some underlying mechanisms of toxicity by the different chemical fractions of ambient particulate matter (PM). This in vitro study sought also to better evaluate and compare the respective toxicities of fine particles (PM) and their inorganic and organic chemical fractions, and the respective toxicities of the organic chemical fractions of PM and quasi-ultrafine particles (PM). Human bronchial epithelial BEAS-2B cells were also exposed for 6-48 h to relatively low doses of PM and their organic extractable (OEM) and non-extractable (NEM) fractions, and the organic extractable fraction (OEM) of PM. We reported that not only PM, but also, to a lesser extent, its inorganic chemical fraction, NEM, and organic chemical fraction, OEM, were able to significantly induce ROS overproduction and oxidative damage notwithstanding the early activation of NRF2 signaling pathway. Moreover, for any exposure, inflammatory and apoptotic events were noticed. Similar results were observed in BEAS-2B cells exposed to OEM, rich of polycyclic aromatic hydrocarbons and their nitrated and oxygenated derivatives. In BEAS-2B cells exposed for 24 and 48 h to OEM and OEM, to a higher extent, there was an alteration of the levels of some critical proteins even though crucial for the autophagy rather than a real reduction of autophagy. It is noteworthy that the toxicological effects were equal or mostly higher in BEAS-2B cells exposed for 6 and/or 24 h to PM from those exposed to NEM or OEM, and in BEAS-2B cells exposed for 6 and/or mostly 24 h to OEM from those exposed to OEM. Taken together, these results revealed the higher potentials for toxicity, closely linked to their respective physical and chemical characteristics, of PM vs NEM and/or OEM, and OEM vs OEM.

摘要

新的毒理学研究仍然迫切需要,以提高目前对环境颗粒物(PM)不同化学部分诱导一些毒性潜在机制的认识。这项体外研究还旨在更好地评估和比较细颗粒物(PM)及其无机和有机化学部分,以及 PM 和准超细微粒(PM)的有机化学部分各自的毒性。人体支气管上皮 BEAS-2B 细胞还分别暴露于相对较低剂量的 PM 及其可提取有机部分(OEM)和不可提取部分(NEM),以及 PM 的可提取有机部分(OEM)6-48 小时。我们报道,不仅 PM,而且其无机化学部分、NEM 和有机化学部分、OEM,尽管早期激活了 NRF2 信号通路,但都能够显著诱导 ROS 过度产生和氧化损伤。此外,对于任何暴露,都会出现炎症和凋亡事件。在暴露于富含多环芳烃及其硝化和氧化衍生物的 OEM 的 BEAS-2B 细胞中观察到了类似的结果。在暴露于 OEM 和 OEM 的 BEAS-2B 细胞中,暴露 24 和 48 小时后,即使对于自噬至关重要,一些关键蛋白的水平也会发生改变,而不是真正减少自噬。值得注意的是,暴露于 PM 的 BEAS-2B 细胞在暴露于 OEM 或 OEM 6 和/或 24 小时后的毒性效应与暴露于 NEM 或 OEM 的 BEAS-2B 细胞相当或更高,而暴露于 OEM 的 BEAS-2B 细胞在暴露于 OEM 6 和/或 24 小时后的毒性效应与暴露于 OEM 的 BEAS-2B 细胞相当或更高。总之,这些结果揭示了 PM 与 NEM 和/或 OEM 相比,以及 OEM 与 OEM 相比,其毒性潜力更高,这与它们各自的物理和化学特性密切相关。

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