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
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DOI：
10.1101/2023.10.24.563735
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发表时间：
2023-10
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影响因子：
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通讯作者：
Sean M. Gettings;William Timbury;Anna Dmochowska;Riddhi Sharma;L. Mackenzie;G. Miquelard-Garnier
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文献类型：
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作者：
Sean M. Gettings;William Timbury;Anna Dmochowska;Riddhi Sharma;L. Mackenzie;G. Miquelard-Garnier
本研究的目的是评估由聚对苯二甲酸乙二醇酯（PET）组成的微米和纳米塑料颗粒对人脑血管周细胞的影响，PET是塑料污染的重要贡献者。具体来说，我们深入研究了它们对线粒体功能，氧化应激以及与氧化应激和铁凋亡相关的基因表达的影响。我们的研究结果表明，将单一培养的人脑血管周细胞在体外暴露于浓度为50 ppm的PET颗粒持续6天不会引起氧化应激。值得注意的是，我们观察到线粒体呼吸的各个方面的增强，包括细胞外酸化，质子泵泄漏，最大呼吸，备用呼吸能力，和ATP生产的周细胞进行PET颗粒。此外，线粒体DNA拷贝数或与氧化应激和铁凋亡相关的基因表达没有统计学显著性改变。这些结果表明，在浓度为百万分之50（ppm）和暴露6天，PET颗粒不会诱导人脑血管周细胞的氧化应激。相反，它们似乎激发了一种潜在的线粒体兴奋效应，也称为线粒体兴奋效应，反应，这似乎增强了线粒体功能。进一步的研究是必要的，以探讨阶段的有丝分裂和塑料的血脑屏障和细胞间相互作用的完整性的潜在后果。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，并强调迫切需要对塑料颗粒的暴露进行持续检查。图形摘要（创建于BioRender.com）突出显示聚对苯二甲酸乙二醇酯（PET）微米和纳米塑料的制造PET颗粒增加周细胞线粒体呼吸功能PET颗粒增加周细胞细胞外酸化在经历PET颗粒的周细胞中未观察到氧化应激
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 and ferroptosis. Our findings demonstrate that the exposure of a monoculture of human brain vascular pericytes to PET particles in vitro at a concentration of 50 ppm for a duration of 6 days did not elicit oxidative stress. Notably, we observed an augmentation in various aspects of mitochondrial respiration, including extracellular acidification, proton pump leakage, maximal respiration, spare respiratory capacity, and ATP production in pericytes subjected to PET particles. Furthermore, there were no statistically significant alterations in mitochondrial DNA copy number, or the expression of genes linked to oxidative stress and ferroptosis. These outcomes suggest that, at a concentration of 50 parts per million (ppm) and for 6 days exposure, PET particles do not induce oxidative stress in human brain vascular pericytes. Instead, they seem to incite a potential mitochondrial hormesis, also named mitohormesis, response, which seemingly enhances mitochondrial function. 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. Graphical Abstract (created with BioRender.com) Highlight Fabrication of polyethylene terephthalate (PET) micro- and nanoplastics PET particles increase pericytes mitochondrial respiration functions PET particles increase pericytes extracellular acidification Oxidative stress was not observed in pericytes subjected to PET particles