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; Institute for Environmental Pollution and Health, School of Environmental and Chemical Engineering, Shanghai University, Shanghai 200444, PR China.
Sci Total Environ. 2020 Jul 15;726:138679. doi: 10.1016/j.scitotenv.2020.138679. Epub 2020 Apr 13.
To understand the toxicity and mechanism of polystyrene microplastics (PS-MPs) exposure, Caenorhabditis elegans (C. elegans) was exposed to various concentrations (0, 0.1, 1, 10, and 100 μg/L) of PS-MPs, and the levels physiological, biochemical, and molecular parameters were measured as endpoints. Subacute exposure to 1-100 μg/L of PS-MPs resulted in adverse physiological effects in C. elegans, and PS-MPs were ingested and accumulated in the intestine of C. elegans. Exposure to 100 μg/L of PS-MPs significantly increased reactive oxygen species (ROS) production, lipofuscin accumulation, and the expression oxidative stress-related genes, which suggests that PS-MPs exposure induced oxidative stress by ROS. In addition, exposure to 100 μg/L of PS-MPs caused a hyperpermeable state of the intestinal barrier and altered the expression of genes related to intestinal development, which indicates intestinal damage in C. elegans. According to Pearson correlation analyses, oxidative stress and intestinal damage were significantly correlated with adverse effects of PS-MPs in C. elegans. Therefore, it was speculated that the toxicity induced by PS-MPs resulted from the combination of oxidative stress and intestinal injury.
为了理解聚苯乙烯微塑料（PS-MPs）暴露的毒性和机制，用不同浓度（0、0.1、1、10 和 100μg/L）的 PS-MPs 暴露秀丽隐杆线虫（C. elegans），并将生理、生化和分子参数水平作为终点进行测量。亚急性暴露于 1-100μg/L 的 PS-MPs 导致 C. elegans 产生不良生理效应，并且 PS-MPs 被摄入并在 C. elegans 的肠道中积累。暴露于 100μg/L 的 PS-MPs 显著增加了活性氧（ROS）的产生、脂褐素的积累和与氧化应激相关的基因的表达，这表明 PS-MPs 暴露通过 ROS 诱导了氧化应激。此外，暴露于 100μg/L 的 PS-MPs 导致肠道屏障的通透性增加，并改变了与肠道发育相关的基因的表达，这表明 C. elegans 中的肠道损伤。根据 Pearson 相关分析，氧化应激和肠道损伤与 PS-MPs 在 C. elegans 中的不良影响显著相关。因此，推测 PS-MPs 引起的毒性是由氧化应激和肠道损伤的共同作用所致。
