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慢性暴露于紫外线老化微塑料通过影响秀丽隐杆线虫中多巴胺、谷氨酸和血清素神经递质传递诱导神经毒性。

Chronic exposure to UV-aged microplastics induces neurotoxicity by affecting dopamine, glutamate, and serotonin neurotransmission in Caenorhabditis elegans.

机构信息

Institute for Environmental pollution and health, School of Environmental and Chemical Engineering, Shanghai University, Shanghai 200444, China; State Environmental Protection Key Laboratory of Environmental Pollution Health Risk Assessment, South China Institute of Environmental Sciences, Ministry of Ecology and Environment, Guangzhou 510655, China.

State Environmental Protection Key Laboratory of Environmental Pollution Health Risk Assessment, South China Institute of Environmental Sciences, Ministry of Ecology and Environment, Guangzhou 510655, China.

出版信息

J Hazard Mater. 2021 Oct 5;419:126482. doi: 10.1016/j.jhazmat.2021.126482. Epub 2021 Jun 24.

DOI:10.1016/j.jhazmat.2021.126482
PMID:34186424
Abstract

Microplastics are ubiquitous in all environments and exert toxic effects in various organisms. However, the neurotoxicity and underlying mechanisms of long-term exposure to MPs aged under UV radiation remain largely unclear. In this study, Caenorhabditis elegans was treated with 0.1-100 μg/L virgin and aged polystyrene microplastics (PS-MPs) for 10 d, with locomotion behavior, neuronal development, neurotransmitter content, and neurotransmission-related to gene expression as endpoints. Using locomotion behavior as an endpoint, chronic exposure to aged PS-MPs at low concentrations (1 μg/L) caused more severe neurotoxicity than that to virgin PS-MPs. In transgenic nematodes, exposure to 10-100 μg/L aged PS-MPs significantly influenced the fluorescence intensity and percentage of worms with neurodegeneration of dopaminergic, glutamatergic, and serotonergic neurons compared with control. Further investigations showed that the content of glutamate, serotonin, and dopamine was significantly influenced in nematodes chronically exposed to 100 μg/L of aged PS-MPs. Similarly, neurotransmission-related gene (e.g., eat-4, dat-1, and tph-1) expression was also altered in nematodes. These results indicate that aged PS-MPs exert neurotoxicity owing to their effects on dopamine, glutamate, and serotonin neurotransmission. This study provides insights into the underlying mechanisms and potential risks of PS-MPs after UV radiation.

摘要

微塑料在所有环境中无处不在,并对各种生物产生毒性作用。然而,在紫外线辐射下老化的 MPs 的神经毒性及其潜在机制在很大程度上仍不清楚。在这项研究中,用 0.1-100μg/L 的原始和老化聚苯乙烯微塑料(PS-MPs)处理秀丽隐杆线虫 10 天,以运动行为、神经元发育、神经递质含量和与神经传递相关的基因表达为终点。以运动行为为终点,慢性暴露于低浓度(1μg/L)的老化 PS-MPs 比暴露于原始 PS-MPs 更严重的神经毒性。在转基因线虫中,与对照组相比,暴露于 10-100μg/L 的老化 PS-MPs 显著影响多巴胺能、谷氨酸能和血清素能神经元的神经退行性变的荧光强度和具有神经退行性变的线虫百分比。进一步的研究表明,慢性暴露于 100μg/L 的老化 PS-MPs 会显著影响线虫中谷氨酸、血清素和多巴胺的含量。同样,与神经传递相关的基因(如 eat-4、dat-1 和 tph-1)的表达也在线虫中发生改变。这些结果表明,老化 PS-MPs 通过对多巴胺、谷氨酸和血清素神经传递的影响发挥神经毒性作用。本研究为 PS-MPs 在紫外线辐射后的潜在机制和潜在风险提供了深入了解。

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