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The mitochondrial fission-mitophagy axis drives neuronal S-phase arrest and hippocampal damage in co-exposure to polystyrene nanoplastics and lead
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Researchers found that polystyrene nanoplastics facilitated lead accumulation in hippocampal neurons via clathrin-mediated endocytosis, and that co-exposure — but not either stressor alone — synergistically triggered S-phase cell cycle arrest, oxidative stress, and memory deficits in mice by driving excessive mitochondrial fission and activating the PINK1/Parkin mitophagy pathway.
Smaller polystyrene nanoplastics (PS-NPs) can act as vectors for co-existing environmental heavy metals like lead (Pb). The complex neurological health risks posed by these co-exposures are concerning, but their combined neurotoxicity mechanism remains unclear. This study investigated the individual and combined toxic impacts of PS-NPs (5 mg/kg in mice, 50 μg/mL in HT22 cells) and Pb (100 mg/L in mice, 10 μg/mL in HT22 cells) on hippocampal neurons, and explored the underlying mechanisms. The results show that PS-NPs facilitate Pb accumulation in the mouse hippocampus and HT22 cells via clathrin-mediated endocytosis. Co-exposure to Pb and PS-NPs, but not either alone, synergistically induced hippocampal neuronal damage, manifesting as synaptic loss and memory deficits in mice, and triggered S-phase cell cycle arrest alongside oxidative stress in HT22 cells. Mechanistically, Pb+PS-NPs caused mitochondrial dysfunction and shifted mitochondrial dynamics towards excessive fission, evidenced by upregulated DRP1/p-DRP1 and downregulated MFN1/2, and activated PINK1/Parkin-mediated mitophagy. Crucially, inhibition of this mitochondrial fission-mitophagy axis by Mitochondrial Division Inhibitor 1 or cyclosporin A attenuated mitochondrial damage, rescued S-phase arrest, and alleviated hippocampal neuronal injury. Our findings unveil a novel pathway wherein the mitochondrial fission-mitophagy axis drives neuronal cell cycle arrest and cognitive impairment, providing new insights into the risks of combined pollutant exposure.
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Co-exposure to PFOA, PFBA and nanoplastics synergistically exacerbates neurotoxicity by impairing PINK1/Parkin-mediated mitophagy
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Researchers investigated the combined neurotoxic effects of two PFAS chemicals (PFOA and PFBA) with nanoplastics using zebrafish and human neuronal cells. They found that co-exposure synergistically worsened neurodevelopmental impairments and behavioral abnormalities by disrupting a key cellular cleanup pathway called PINK1/Parkin-mediated mitophagy. The study suggests that nanoplastics can amplify the neurotoxicity of PFAS compounds by impairing the cells' ability to clear damaged mitochondria.
Polystyrene nanoplastics induce cognitive dysfunction and dendritic spine deterioration via excessive mitochondrial fission
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Researchers demonstrated that polystyrene nanoplastics can cross the blood-brain barrier and accumulate in mouse brains, leading to cognitive impairment and loss of connections between brain cells. The damage was driven by excessive splitting of mitochondria, the energy-producing structures within cells, which triggered runaway cellular cleanup processes. Importantly, a drug that blocks this mitochondrial splitting reversed the cognitive damage, suggesting a potential therapeutic approach to nanoplastic-related brain injury.
Polystyrene nanoplastics induce hippocampal damage and cognitive deficits through oxidative stress-triggered microglial extracellular traps and neuronal ferroptosis
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Researchers showed that polystyrene nanoplastics impair spatial memory in mice by triggering a cascade in which hippocampal oxidative stress activates microglia to release extracellular traps, sustaining neuroinflammation that drives neuronal ferroptosis — a form of iron-dependent cell death — and that the antioxidant N-acetylcysteine blocks this entire pathway and preserves cognitive function.
Polystyrene nanoplastics exposure induces cognitive impairment in mice via induction of oxidative stress and ERK/MAPK-mediated neuronal cuproptosis
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This mouse study found that polystyrene nanoplastics caused cognitive impairment by triggering oxidative stress and activating a cell-death process called cuproptosis in brain neurons. The findings suggest that copper buildup and specific signaling pathways may be therapeutic targets for reducing brain damage from nanoplastic exposure, though these results still need to be confirmed in human-relevant models.
Polystyrene exacerbates cadmium‐induced mitochondrial damage to lung by blocking autophagy in mice
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Researchers found that polystyrene microplastics exacerbated cadmium-induced mitochondrial damage in mouse lungs by blocking autophagy, revealing a synergistic toxicity mechanism when these two common environmental contaminants co-occur.
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