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Amino-Functionalized Polystyrene Nano-Plastics Induce Mitochondria Damage in Human Umbilical Vein Endothelial Cells.
Fu, Yiqi; Fan, Mengqi; Xu, Liwang; Wang, Hui; Hu, Qinglian; Jin, Yuanxiang.
  • Fu Y; College of Biotechnology and Bioengineering, Zhejiang University of Technology, Hangzhou 310032, China.
  • Fan M; College of Biotechnology and Bioengineering, Zhejiang University of Technology, Hangzhou 310032, China.
  • Xu L; College of Biotechnology and Bioengineering, Zhejiang University of Technology, Hangzhou 310032, China.
  • Wang H; College of Biotechnology and Bioengineering, Zhejiang University of Technology, Hangzhou 310032, China.
  • Hu Q; College of Biotechnology and Bioengineering, Zhejiang University of Technology, Hangzhou 310032, China.
  • Jin Y; College of Biotechnology and Bioengineering, Zhejiang University of Technology, Hangzhou 310032, China.
Toxics ; 10(5)2022 Apr 25.
Article en En | MEDLINE | ID: mdl-35622629
ABSTRACT
As emerging contaminants, nano-plastics have become a major cause for concern for their adverse effects on the ecosystem and human health. The nano-sized properties of nano-plastics enable their exposure risks to humans through the food chain or other ways. However, the fate and adverse impact of nano-plastics on the human cardiovascular system are lacking. In this regard, the human umbilical vein endothelial cell line HUVEC was applied as a cell model to investigate the biological effects of noncharged polystyrene nano-plastics (PS NPs) and amino-functionalized nano-plastics (NH2-PS NPs). The positively charged PS NPs exhibited higher cytotoxicity to HUVEC, as evidenced by the decreased cell viability, enhanced ROS generation, and decreased mitochondria membrane potential triggered by NH2-PS NPs. Importantly, RT-PCR analysis revealed that NH2-PS NPs dysregulated the mitochondrial dynamics, replication, and function-related gene expression. This study demonstrated that NH2-PS NPs presented higher risks to endothelial cells than non-charged nano-plastics by interfering with mitochondria, which supported the direct evidence and expanded the potential risks of PS NPs.
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