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Amino-Functionalized Polystyrene Nano-Plastics Induce Mitochondria Damage in Human Umbilical Vein Endothelial Cells
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Researchers found that amino-functionalized polystyrene nanoplastics can damage mitochondria in human umbilical vein endothelial cells, which line blood vessels. The study suggests that nanoplastics small enough to enter the body through the food chain may pose risks to the cardiovascular system by disrupting cellular energy production and triggering oxidative stress in vascular cells.
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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Researchers exposed human vascular endothelial cells to polystyrene microplastics at concentrations comparable to levels detected in human blood. They found that the microplastics caused oxidative stress, reduced antioxidant defenses, and triggered apoptosis in the vascular cells. The study suggests that microplastics circulating in the bloodstream at realistic concentrations may contribute to vascular damage by impairing cellular protective mechanisms.
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Researchers investigated how polystyrene microplastics affect human heart muscle cells at concentrations reflecting estimated daily human intake levels. They found that the microplastics caused oxidative stress, mitochondrial dysfunction, and disrupted calcium signaling in the cells. The study suggests that microplastic exposure may contribute to cardiovascular risks by directly damaging heart cell function at the cellular level.
Impact of Micro- and Nanoplastics on Mitochondria
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This review examines how micro- and nanoplastics can damage mitochondria, the energy-producing structures inside cells that are critical for metabolism and cell survival. Researchers found that plastic particle exposure can trigger oxidative stress, disrupt mitochondrial membrane function, and interfere with energy production pathways. Since mitochondrial dysfunction is linked to numerous health conditions, the study suggests this may be a key mechanism through which plastic pollution affects human health.
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