聚对苯二甲酸乙二醇酯(PET)微塑料颗粒和纳米塑料颗粒在不诱导氧化应激的情况下影响人脑血管周细胞线粒体的效率

IF 4.7 3区 环境科学与生态学 Q2 ENVIRONMENTAL SCIENCES
Sean M. Gettings , William Timbury , Anna Dmochowska , Riddhi Sharma , Rebecca McGonigle , Lewis E. MacKenzie , Guillaume Miquelard-Garnier , Nora Bourbia
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引用次数: 0

摘要

这项研究的目的是评估由聚对苯二甲酸乙二醇酯(PET)组成的微塑料颗粒和纳米塑料颗粒对人脑血管周细胞的影响。具体来说,我们研究了它们对线粒体功能、氧化应激以及与氧化应激、铁变态反应和线粒体功能相关的基因表达的影响。我们的研究结果表明,在体外将单细胞培养的人脑血管周细胞暴露于浓度为 50 μg/ml 的 PET 粒子中 3、6 和 10 天,不会引起氧化应激。值得注意的是,我们观察到 PET 粒子作用 3 天的血管周细胞线粒体呼吸的各个方面,包括最大呼吸量、剩余呼吸量和 ATP 产量都有所下降,而线粒体功能在 6 天和 10 天后有所恢复。此外,线粒体DNA拷贝数以及与氧化应激和铁变态反应相关的基因表达没有发生统计学意义上的显著变化,但线粒体转录因子A(TFAM)基因的表达在暴露3天时有所增加。相反,暴露 3 天后,PET 会损害线粒体功能,但暴露 6 天后又会恢复。这似乎表明潜在的线粒体激素生成反应(mitohormesis)被激发,涉及基因 TFAM。我们有必要开展进一步研究,探讨线粒体激素生成的各个阶段以及塑料对血脑屏障完整性和细胞间相互作用的潜在影响。这项研究有助于我们理解纳米塑料污染对人类健康的潜在影响,并强调了对塑料微粒暴露进行持续检查的迫切需要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Polyethylene terephthalate (PET) micro- and nanoplastic particles affect the mitochondrial efficiency of human brain vascular pericytes without inducing oxidative stress

Polyethylene terephthalate (PET) micro- and nanoplastic particles affect the mitochondrial efficiency of human brain vascular pericytes without inducing oxidative stress

The objective of this investigation was to evaluate the influence of micro- and nanoplastic particles composed of polyethylene terephthalate (PET), a significant contributor to plastic pollution, on human brain vascular pericytes. Specifically, we delved into their impact on mitochondrial functionality, oxidative stress, and the expression of genes associated with oxidative stress, ferroptosis and mitochondrial functions. Our findings demonstrate that the exposure of a monoculture of human brain vascular pericytes to PET particles in vitro at a concentration of 50 μg/ml for a duration of 3, 6 and 10 days did not elicit oxidative stress. Notably, we observed a reduction in various aspects of mitochondrial respiration, including maximal respiration, spare respiratory capacity, and ATP production in pericytes subjected to PET particles for 3 days, with a mitochondrial function recovery at 6 and 10 days. Furthermore, there were no statistically significant alterations in mitochondrial DNA copy number, or in the expression of genes linked to oxidative stress and ferroptosis, but an increase of the expression of the gene mitochondrial transcription factor A (TFAM) was noted at 3 days exposure.

These outcomes suggest that, at a concentration of 50 μg/ml, PET particles do not induce oxidative stress in human brain vascular pericytes. Instead, at 3 days exposure, PET exposure impairs mitochondrial functions, but this is recovered at 6-day exposure. This seems to indicate a potential mitochondrial hormesis response (mitohormesis) is incited, involving the gene TFAM. Further investigations are warranted to explore the stages of mitohormesis and the potential consequences of plastics on the integrity of the blood-brain barrier and intercellular interactions. This research contributes to our comprehension of the potential repercussions of nanoplastic pollution on human health and underscores the imperative need for ongoing examinations into the exposure to plastic particles.

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来源期刊
NanoImpact
NanoImpact Social Sciences-Safety Research
CiteScore
11.00
自引率
6.10%
发文量
69
审稿时长
23 days
期刊介绍: NanoImpact is a multidisciplinary journal that focuses on nanosafety research and areas related to the impacts of manufactured nanomaterials on human and environmental systems and the behavior of nanomaterials in these systems.
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