College of Chemistry, Chemical Engineering and Materials Science, Key Laboratory of Molecular and Nano Probes, Ministry of Education, Shandong Normal University, Jinan 250014, China; CAS Key Laboratory of Coastal Environmental Processes and Ecological Remediation, Yantai Institute of Coastal Zone Research, Chinese Academy of Sciences, Yantai 264003, China.
CAS Key Laboratory of Coastal Environmental Processes and Ecological Remediation, Yantai Institute of Coastal Zone Research, Chinese Academy of Sciences, Yantai 264003, China; Center for Ocean Mega-Science, Chinese Academy of Sciences, Qingdao 266071, China.
J Hazard Mater. 2021 Mar 15;406:124306. doi: 10.1016/j.jhazmat.2020.124306. Epub 2020 Oct 19.
Nanoplastics have recently become a worldwide concern as newly emerging airborne pollutants, which can associate with polycyclic aromatic hydrocarbons (PAHs) and form combined contaminant nanoparticles (CCNPs). After being inhaled in the respiratory system, the CCNPs would first encounter the mucous gel layer being rich in mucin. Herein, polystyrene-benzopyrene (PS@Bap) NPs were prepared as CCNPs model and their interaction with mucin and the resultant biological responses were studied. It was observed that mucin corona stably attached to the CCNPs surface, which significantly altered the fate of the CCNPs in lung epithelial cells (A 549 cell line). The mucin corona would 1) stably adsorbed on PS@Bap at the early stages of endocytosis until degraded during the lysosomal transport and maturation process, 2) delay intracellular trafficking of PS@Bap and the progress of Bap detached from PS, 3) enhance uptake of PS@Bap but reduce the cytotoxicity elicited by PS@Bap, as indicated by cell viability, generation of reactive oxygen species, impairment on mitochondrial function, and further cell apoptosis. In addition, in vivo study also verified the enhanced effect of PS on the development of an acute lung inflammatory response induced by Bap. This study highlights the significance of incorporating the effects of mucin for precisely assessing the respiratory system toxicity of nanoplastics based CCNPs in atmospheric environments.
纳米塑料作为新兴的空气污染物，已引起全球关注，它们可以与多环芳烃（PAHs）结合形成复合污染物纳米颗粒（CCNPs）。吸入呼吸道后，CCNPs 首先会遇到富含粘蛋白的粘液凝胶层。在此，制备了聚苯乙烯-苯并芘（PS@Bap）纳米颗粒作为 CCNPs 模型，研究了它们与粘蛋白的相互作用及由此产生的生物学反应。结果表明，粘蛋白冠稳定地附着在 CCNPs 表面，这显著改变了 CCNPs 在肺上皮细胞（A549 细胞系）中的命运。粘蛋白冠 1）在胞吞作用的早期阶段稳定地吸附在 PS@Bap 上，直到在溶酶体运输和成熟过程中降解，2）延迟 PS@Bap 的细胞内转运和 Bap 从 PS 上脱离的进展，3）增强 PS@Bap 的摄取，但降低 PS@Bap 引起的细胞毒性，如细胞活力、活性氧的产生、线粒体功能的损害和进一步的细胞凋亡所表明的。此外，体内研究还验证了 PS 对 Bap 诱导的急性肺炎症反应发展的增强作用。本研究强调了在大气环境中，为了更准确地评估基于 CCNPs 的纳米塑料对呼吸系统的毒性，需要考虑粘蛋白的影响。
