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Amine-modified polystyrene particles induce surface chemistry-driven immunotoxicity in microglia: Protective effects of trolox
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Researchers found that amine-modified polystyrene microplastics were significantly more toxic to brain immune cells (microglia) than plain or carboxyl-modified polystyrene at the same concentration. The modified particles triggered strong inflammatory responses, mitochondrial damage, and oxidative stress that also led to secondary damage in nearby neurons. Treatment with Trolox, a vitamin E analog, reduced the toxic effects by suppressing inflammatory signaling pathways.
Microplastics are increasingly prevalent environmental contaminants that pose potential risks to human health, particularly affecting the central nervous system. This study investigated the mechanisms by which surface modification of polystyrene microplastics affects their neurotoxicity in microglial cells. The results indicated that amine-modified polystyrene (PS-NH) microplastics induce substantially higher cytotoxicity in BV2 microglial cells than that by plain polystyrene or carboxyl-modified polystyrene at the same concentration. PS-NH particles were rapidly internalized by microglia, inducing pronounced inflammatory responses, including elevated expression of proinflammatory cytokines (TNF-α and IL-6) and M1 polarization markers. Furthermore, our findings indicated that PS-NH induced mitochondrial damage accompanied by sustained superoxide accumulation, which led to cellular oxidative stress associated with nitric oxide synthesis and apoptosis. Mitochondrial superoxide production, particularly via complex II and III inhibition, is a critical mechanism underlying the enhanced toxicity of PS-NH. Furthermore, PS-NH-induced microglial cytotoxicity contributed to the secondary degeneration of surrounding neuronal cells. Treatment with Trolox, a vitamin E analog, attenuated microglial toxicity and neuronal loss through suppression of ROS-mediated inflammatory signaling, including reduced JNK phosphorylation, NLRP3 expression, and NF-κB p50 nuclear translocation. These results highlight the importance of surface chemistry in determining microplastic toxicity and indicate that amine modification substantially enhances the neuroinflammatory and neurotoxic potential of microplastics through pathways mediated by mitochondrial reactive oxygen and nitrogen species. These findings have important implications for assessing the risks of microplastics in neurological disorders and for developing strategies to mitigate their harmful effects.
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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.
Neurotoxic effects of polystyrene nanoplastics on memory and microglial activation: Insights from in vivo and in vitro studies
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In a mouse study, tiny nanoplastics (30-50 nanometers) that were swallowed reached the brain and caused memory problems by activating the brain's immune cells, called microglia, which triggered inflammation. This is concerning because it shows that nanoplastics small enough to be found in everyday products like cosmetics could cross into the brain and impair cognitive function.
Microglial phagocytosis of polystyrene microplastics results in immune alteration and apoptosis in vitro and in vivo
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Researchers found that polystyrene microplastics can cross the blood-brain barrier in mice after oral exposure and accumulate in brain tissue, where they are engulfed by microglia, the brain's immune cells. This engulfment triggered inflammatory responses and cell death in the microglia both in cell cultures and in living mice. The study suggests that microplastic exposure may affect brain immune function, with potential implications for neurological health.
Surface functionalization-dependent inflammatory potential of polystyrene nanoplastics through the activation of MAPK/ NF-κB signaling pathways in macrophage Raw 264.7
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Researchers studied how surface chemistry of polystyrene nanoplastics affects their ability to trigger inflammation in immune cells. They found that amino-functionalized nanoplastics caused the strongest inflammatory response by activating the MAPK and NF-kB signaling pathways and generating reactive oxygen species. The study demonstrates that the chemical coating on nanoplastics significantly determines their potential to cause immune system disruption.
Cerebral neurotoxicity of amino-modified polystyrene nanoplastics in mice and the protective effects of functional food Camellia pollen
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Mice exposed long term to amino-modified polystyrene nanoplastics had the particles in brain tissue, along with higher activity of two genes associated with Alzheimer's disease. In cell experiments, the particles disrupted proteins that seal the blood-brain barrier and promoted a modified form of tau. Camellia pollen reduced these effects in the cell models.
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