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Polystyrene Microsphere Exposure Disrupts Mitochondrial Redox and Induces Mitochondrial Impairment in Human Pluripotent NTERA-2 cl.D1 Cells.
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Human stem cells grown in a lab dish were exposed to tiny polystyrene plastic particles for 24 hours. The particles entered the cells, increased harmful molecules called reactive oxygen species, and disrupted the cells' mitochondria, the parts that produce energy, affecting their function and membrane health.
The increased demand for plastic products in the economy resulted in the inherent generation of tiny plastic particles to the environment which are collectively termed as the 'microplastics' (MPs). MPs are emerging environmental contaminants that enter the human body via inhalation, ingestion, skin contact, and human food chain accumulation. Once localised within the cells, they critically affect the cellular energy kinetics. In this study investigated the cytotoxicity effects and mitochondrial function in polystyrene microplastics (PS-MPs) treated human pluripotent cells; NTERA2 cl. D1 cells. Briefly, NTERA2 CL. D1 cells; were exposed to fluorescent PS-MPs of size 1µm for 24h. Cellular localisation, total cellular ROS and mitochondrial ROS (mtROS), and mitochondrial membrane potential, were evaluated using fluorescence imaging, flow cytometry, and qRT‑PCR. Our results demonstrated that PS-MPs internalised human pluripotent cells dose-dependently after 24h exposure and elevated the total cellular ROS resulting in oxidative stress. Additionally, the microplastics also generated mitochondrial ROS which reduced healthy mitochondrial population and hampered the mitochondrial membrane potential. Moreover, gene expression analysis of the microplastics treatment group revealed possible mitohormetic response accompanied by significant alteration in mitochondrial fission and fusion. Additionally, these alterations further resulted in mitochondrial dysfunction in the microplastics treatment group. Collectively, our findings provide novel evidence that PS-MPs disrupt mitochondrial function in human pluripotent cells by influencing mitochondrial membrane potential.
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