Guangdong Provincial Key Laboratory of High-Quality Recycling of End-of-Life New Energy Devices, Guangzhou Institute of Energy Conversion, Chinese Academy of Sciences, Guangzhou 510630, 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.
Sci Total Environ. 2024 Nov 20;952:175939. doi: 10.1016/j.scitotenv.2024.175939. Epub 2024 Aug 30.
The use of plastic bowls (PB) has garnered increasing scrutiny due to the inevitable generation of microplastics (MPs) throughout their lifecycle. Despite this concern, there exists a limited understanding of the behaviors, toxicological effects, and mechanisms associated with aged PB (A-PB). This research investigated the photoaging properties of A-PB following ultraviolet irradiation and evaluated the neurotoxic impact of exposure to A-PB at environmentally relevant concentrations (0.001-1 mg/L) on Caenorhabditis elegans. Significant alterations in the crystallinity, elemental composition, and functional groups of A-PB were observed compared to virgin PB (V-PB), along with the emergence of environmentally persistent free radicals and reactive oxygen species. Toxicity assessments revealed that exposure to 0.1-1 mg/L A-PB induced greater neurotoxicity on locomotion behaviors compared to V-PB, as evidenced by marked reductions in head thrashes, body bends, wavelength, and mean amplitude. Exposure to A-PB also altered the fluorescence intensities and neurodegeneration percentage of dopaminergic, serotonergic, and GABAergic neurons, suggesting neuronal damage in the nematodes. Correspondingly, decreases in the levels of dopamine, serotonin, and GABA were noted together with significant drops in the expression of neurotransmitter-related genes (e.g., dat-1, tph-1, and unc-47). Correlation analyses established a significant positive relationship between these genes and locomotion behaviors. Further exploration showed the absence of locomotion behaviors in dat-1 (ok157), tph-1 (mg280), and unc-47 (e307) mutants, underscoring the pivotal roles of the dat-1, tph-1, and unc-47 genes in mediating neurotoxicity in C. elegans. This study sheds light on the photoaging characteristics and heightened toxicity of A-PB, elucidating the mechanisms driving A-PB-induced neurotoxicity.
由于在其整个生命周期中不可避免地会产生微塑料（MPs），因此人们对塑料碗（PB）的使用越来越关注。尽管存在这种担忧，但对于老化的 PB（A-PB）的行为、毒理学效应和机制，人们的了解仍然有限。本研究调查了紫外线照射后 A-PB 的光老化特性，并评估了在环境相关浓度（0.001-1mg/L）下暴露于 A-PB 对秀丽隐杆线虫的神经毒性影响。与原始 PB（V-PB）相比，A-PB 的结晶度、元素组成和官能团发生了显著变化，同时出现了环境持久性自由基和活性氧。毒性评估显示，与 V-PB 相比，暴露于 0.1-1mg/L 的 A-PB 对运动行为的神经毒性更大，表现在头部抽搐、身体弯曲、波长和平均幅度明显减少。暴露于 A-PB 还改变了多巴胺能、血清素能和 GABA 能神经元的荧光强度和神经退行性病变百分比，表明线虫神经元受损。相应地，注意到多巴胺、血清素和 GABA 的水平下降，以及与神经递质相关的基因（例如，dat-1、tph-1 和 unc-47）的表达显著下降。相关性分析表明，这些基因与运动行为之间存在显著的正相关关系。进一步的探索表明，dat-1（ok157）、tph-1（mg280）和 unc-47（e307）突变体中没有运动行为，突出了 dat-1、tph-1 和 unc-47 基因在介导秀丽隐杆线虫神经毒性中的关键作用。本研究揭示了 A-PB 的光老化特征和更高的毒性，阐明了驱动 A-PB 诱导神经毒性的机制。
