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Effects of Microplastics on Cell Viability, Phagocytic Activity and Oxidative Stress in Human Peripheral Blood Mononuclear Cells

Preprints.org 2025
Harripriya Sivarathan, Teshan Chathuranga, Aruna Dharshan De Silva, Yohan Lasantha Mahagamage, Maheshi Sasika Mapalagamage

Summary

Researchers exposed human peripheral blood mononuclear cells (PBMCs) to four concentrations of polyethylene glycol and natural microplastics and measured cell viability, phagocytic activity, and oxidative stress. Higher microplastic concentrations reduced cell viability and phagocytic function while increasing oxidative stress markers, indicating that microplastics impair immune cell performance.

Polymers
Body Systems

Microplastics (MPs) are synthetic solid polymers (1µm – 5mm) which are non-biodegradable. The toxicological effects of MPs have been well investigated, but research on how these particles affect PBMCs leaves much to be explored. Different concentrations 0.5 µg/ml, 5 µg/ml, 50 µg/ml, 500 µg/ml of PEG and manually grinded natural MPs were exposed to PBMCs in RPMI medium for 24 hours. Cell viability assay, Neutral Red phagocytosis assay, Griess colorimetric assay, Nitroblue Tetrazolium test was done to examine the cytotoxic effect of MPs on PBMCs. The present study results indicated that both natural MPs and Polyethylene Glycol (PEG) significantly reduced cell viability in a concentration-dependent manner. At highest concentrations, Natural MPs induced phagocytic activity of PBMCs. These MPs may act as stimulants to increase phagocytic activity. Regarding oxidative stress, Natural MPs exposure with PBMCs showed a significant increase in ROS production, whereas PEG exposure didn’t induce notable ROS production. NO production levels remained unchanged in PBMCs after exposure to both PEG and Natural MPs, showing that under the tested conditions, neither treatment significantly influenced the NO-mediated inflammatory pathways. In summary, this present study showed that MPs exposure to humans can impair cell viability, induce phagocytosis and induce ROS production without altering the NO mediated inflammatory pathways.

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