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Primary astrocytes as a cellular depot of polystyrene nanoparticles
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Researchers found that astrocytes — support cells in the brain — absorb polystyrene nanoplastics far more efficiently than neurons and act as a cellular buffer to protect nerve cells, but become overactivated when the particle load is too high, losing their protective function and potentially contributing to neurological harm.
The continuous increase in plastic production has resulted in increased generation of microplastic particles (MPs), and nanoplastic particles (NPs). Recent evidence suggests that nanoplastics may be a potent neurotoxin because they are able to freely cross the blood-brain barrier and enter the brain. Therefore, the cytotoxic effects of polystyrene nanoparticles (PS-NPs) on cellular systems of cerebral origin should be thoroughly investigated. The aim of the current study is to evaluate the cytotoxic potential of 25 nm PS-NPs on in vitro cultured cells such as primary astrocytes, neurons and their co-cultures established from the cerebral cortex of Wistar pups. The results show that PS-NPs are internalized in both neurons and astrocytes, inducing time- and concentration-dependent cytotoxic effects. However, quantification of fluorescence intensity indicates cell type-dependent differences in the efficiency of PS-NPs uptake. Astrocytes are several times more efficient at accumulating PS-NPs than neurons, and this is a phagocytosis-dependent process. Moreover, the high rate of PS-NPs internalization during prolonged exposure (72 h) promotes astroglial activation, as assessed by analysis of GFAP expression and immunocytochemical imaging. The results show that astroglia act as a cellular depot of PS-NPs to protect neurons. However, once the critical threshold is exceeded, astroglia become overactivated and can lose their protective functions. These results highlight the importance of further research on the mechanisms underlying nanoplastic-induced cellular toxicity, which may have implications for understanding the broader impact of plastic pollution on neurological functions.
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Neurotoxic potential of polystyrene nanoplastics in primary cells originating from mouse brain
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Researchers exposed three types of primary mouse brain cells to 100 nm polystyrene nanoplastics and found that neurons underwent apoptosis while astrocytes survived but developed reactive astrocytosis with elevated inflammatory markers, suggesting that neuronal vulnerability to nanoplastic accumulation may be amplified by astrocyte-driven neuroinflammation.
Polystyrene Micro- and Nanoplastic Exposure Triggers an Activation and Stress Response in Human Astrocytes
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Researchers exposed primary human astrocytes to polystyrene micro- and nanoplastics and found that these particles triggered cellular stress responses, including increased production of reactive oxygen species and activation of inflammatory pathways. Nanoplastics were particularly effective at penetrating cells and disrupting normal astrocyte function. The findings suggest that plastic particle exposure may contribute to neuroinflammatory processes in the brain, warranting further investigation into potential neurotoxic effects.
Adverse interactions of plastic nanoparticles with cultured primary microglial cells.
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Tiny plastic particles from broken-down polystyrene (a common plastic) can get absorbed into brain immune cells called microglia, causing stress damage and triggering inflammation, according to lab tests on these cells. This matters because microglia act as the brain's cleanup crew and first line of defense, so if microplastics cause them to malfunction, it could contribute to brain inflammation linked to neurological problems—though this study was done in isolated cells, not in living people, so more research is needed to know exactly what this means for human brain health.
Alleviation of neurotoxicity induced by polystyrene nanoplastics by increased exocytosis from neurons
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Researchers investigated how polystyrene nanoplastics accumulate in neurons and cause toxic effects on brain cells. They found that inhibiting a specific protein involved in transporting particles within cells promoted the export of nanoplastics from neurons, reducing their harmful effects. The study suggests that enhancing the cell's natural ability to expel nanoplastics could be a potential strategy for alleviating their neurotoxic impact.
Polystyrene nanoplastic-encapsulated extracellular vesicles promote blood-brain barrier breakdown and accumulate in the brain.
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Researchers found that extracellular vesicles encapsulating polystyrene nanoplastics prolonged intracellular retention in human endothelial cells, caused a 2.8-fold greater decline in blood-brain barrier electrical resistance than free nanoplastics alone, and promoted brain accumulation in vivo — implicating vesicle-mediated transport as a significant route for nanoplastic neurological entry.
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