Amino-Functionalized Polystyrene Nano-Plastics Induce Mitochondria Damage in Human Umbilical Vein Endothelial Cells

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.

Impact of mucus modulation by N-acetylcysteine on nanoparticle toxicity

“…Having this in mind, NAC is expected to attenuate stressor induced oxidative stress due to its antioxidative properties. As polystyrene nanoparticle induced toxicity might be mediated by oxidative stress ( Fu et al, 2022 ), NAC is expected to rather mitigate any nanoparticle induced toxicity. Given the nanoparticle penetration enhancing property of NAC, the increased cytotoxicity values observed after NAC treatment might rather be attributed to an elevated exposure of cells to an increased number of particles.…”

A Multisystemic Approach Revealed Aminated Polystyrene Nanoparticles‐Induced Neurotoxicity

“…In line with our findings, a previous study in HUVEC cells, reported that PS‐NH 2 NPs affect the MMP more than plain PS NPs. [ 56 ] Another study in cells of the respiratory tract also detected mitochondrial damage upon treatment with PS‐NH 2 only but could also observe an increase in ROS production. [ 5 ] Different from our findings instead, previous work in other cell lines, have shown increased ROS production after treatment with PS NPs (40 nm), however used particles were slightly smaller and bought from a different manufacturer.…”

Nanoparticles‐induced potential toxicity on human health: Applications, toxicity mechanisms, and evaluation models

“…Huang et al 244 showed that decabromodiphenylethane and ZnO-NPs reduced mitochondrial membrane potential (MMP), increased cytochrome C release, and modulated Bax/Bcl-2 and cysteine by disrupting mitochondrial kinetic homeostasis Apoptosis was induced by the expression of dp-3 mRNA and protein. Fu et al 245 showed that amino-functionalized PS-NPs induced mitochondrial damage and decreased cell viability in human umbilical vein endothelial cells. This is consistent with the study by Li et al 246 that PS microplastics trigger mitochondrial damage and apoptosis through ROS-driven calcium overload.…”

“…Fu et al. 245 showed that amino‐functionalized PS–NPs induced mitochondrial damage and decreased cell viability in human umbilical vein endothelial cells. This is consistent with the study by Li et al.…”