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Repeated Polystyrene Nanoplastic Exposure Alters the Redox Balance and Inflammatory Signaling in the Lymphatic Endothelial Cells
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Lab-grown mouse lymph node cells were repeatedly exposed to plastic nanoparticles over 15 days. Cells did not die, but they showed signs of stress, including increased harmful molecules, loss of protective substances, and shifting patterns of inflammation-related proteins over time.
Environmental exposure to nanoplastics (NPLs) is an emerging concern for human health, yet their effects on lymphatic endothelium remain poorly understood. We investigated the effects induced by repeated exposure of the murine lymph node endothelial cells (SVEC4-10 cell line) to polystyrene NPLs (PS-NPLs) at 1.6, 16, and 160 μg/mL over 15 days. PS-NPLs have been characterized in terms of hydrodynamic diameter and polydispersity by dynamic light scattering. Cell viability remained unchanged, while repeated exposure induced a pronounced oxidative stress response, characterized by increased reactive oxygen species (ROS), protein and lipid oxidation, and depletion of reduced glutathione. Nitric oxide levels increased modestly (22.8–30.6%) at the highest concentration. Inflammatory responses were temporally regulated, with early increases in TNFα and IL-1β levels, followed by partial normalization, whereas IL-6 expression showed delayed elevation. Hsp27, Hsp60, Hsp70, and Hsp90 expressions displayed changes consistent with activation of cellular stress-response pathways. Overall, repeated PS-NPL exposure induced a dynamic oxidative stress response and temporally regulated inflammatory alterations, without a significant decrease in cell viability. The temporal modulation of these responses may reflect compensatory cellular processes during prolonged exposure, although the specific mechanisms underlying this response remain to be established.
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Fish skin cells grown in a lab were exposed to polystyrene nanoplastics for 15 days. The cells did not die or change shape, but nanoplastics built up inside them and their membrane fats changed composition, along with increased stress-related chemical activity, without triggering cell death.
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Researchers assessed the effects of polystyrene nanoplastics on adipose stromal cells from pig tissue, finding reduced cell viability after prolonged exposure, increased inflammatory marker TNF-alpha, and elevated oxidative stress markers. These results suggest nanoplastics can disrupt cellular redox homeostasis in adipose tissue at environmentally relevant conditions.
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Mouse embryonic fibroblasts exposed to polystyrene nanoplastics internalized particles via endocytosis without losing viability, but showed activation of antioxidant and autophagic stress pathways, suggesting subcellular dysfunction even in the absence of cell death.
Enhancement of biological effects of oxidised nano- and microplastics in human professional phagocytes
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Researchers studied how virgin and environmentally aged polystyrene nano- and microplastics affect human immune cells (monocytes and macrophages). The study found that oxidized particles, which simulate environmental aging, caused significantly greater DNA damage and oxidative stress than virgin particles, suggesting that weathered plastics in the environment may pose higher health risks.
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Researchers exposed single-celled marine organisms called foraminifera to three types of engineered nanoparticles — including polystyrene nanoplastics — and found that all three accumulated inside the cells and triggered oxidative stress (a form of cellular damage). This study shows that even microscopic seafloor organisms are vulnerable to nanoplastic pollution, expanding the known range of species harmed by plastic contamination.
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