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Polystyrene nanoplastics enhance lead-induced ferroptosis in HT22 cells via clathrin-mediated endocytosis
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Tiny plastic particles called nanoplastics can act like a "Trojan horse," sneaking extra lead into brain cells and making the lead's damage worse, according to a lab study on mouse neurons. Together, plastics and lead triggered more cell death than either alone, raising concerns about real-world exposure to both pollutants at once. More research is needed to confirm this happens in living animals or humans.
The co-occurrence of nanoplastics and heavy metals like lead (Pb) in the environment presents a significant neurotoxic risk, yet the mechanistic basis for their combined effects remains poorly defined. In this study, we investigated the combined neurotoxic effects of 50 nm polystyrene nanoplastics (PS-NPs) and Pb in mouse hippocampal HT22 cells. Co-exposure to PS-NPs (50 μg/mL) and Pb (10 μg/mL)-concentrations commonly used in in vitro mechanistic studies-for 24 h, but not individual treatments, enhanced cytotoxicity and induced ferroptosis-related features, including iron metabolism dysregulation, lipid peroxidation, antioxidant defense impairment, and mitochondrial damage. Furthermore, the ferroptosis inhibitor Ferrostatin-1 (Fer-1) attenuated cell death, supporting ferroptosis as an important contributor to the observed cytotoxicity. Transcriptomic analysis revealed significant alterations in ferroptosis-related pathways, with selected differentially expressed genes validated by qRT-PCR. Physicochemical characterization (DLS/zeta potential) revealed changes in the hydrodynamic size and zeta potential of PS-NPs following incubation with Pb, while ICP-OES analysis of the supernatant provided evidence for the association of Pb with PS-NPs. This enhanced toxicity was associated with increased intracellular Pb accumulation facilitated by PS-NPs, involving the clathrin-mediated endocytosis (CME) pathway, as indicated by upregulation of key CME-related proteins (CHC, AP2M1, and Dynamin 2) and enhanced CHC-AP2M1 co-localization. Pharmacological inhibition of CME using chlorpromazine (CPZ) effectively reduced Pb uptake and attenuated ferroptosis-related cellular damage. Our findings provide insights into a proposed CME-associated Trojan horse-like mechanism whereby PS-NPs enhance ferroptosis-related neuronal responses to Pb exposure, highlighting the potential implications of nanoplastic-heavy metal co-exposure for environmental health.
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Researchers found that polystyrene nanoplastics exacerbated lead-induced liver toxicity in mice, with co-exposure causing higher lead accumulation, more severe inflammation, increased oxidative stress, and greater disruption of protective Nrf2 signaling pathways compared to lead alone.
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Researchers studied how polystyrene nanoplastics and lead, a toxic heavy metal, interact when earthworm immune cells are exposed to both simultaneously at environmentally realistic concentrations. The combined exposure caused more severe cell damage, oxidative stress, and inflammation than either pollutant alone. The findings suggest that nanoplastics can increase the harmful effects of heavy metals on soil organisms, raising concerns about the real-world impact of mixed contaminant exposure.
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Scientists found that when tiny plastic particles (microplastics) and cadmium, a toxic heavy metal, team up, they cause more cell damage and stress in fish than either one does alone, acting like a "Trojan horse" that helps the metal get into the body. Even after exposure stopped, the fish didn't fully recover. This matters because it suggests microplastics in our environment could be secretly carrying and worsening the effects of other pollutants, raising questions about the combined risks we face from eating contaminated fish or being exposed to both pollutants together.
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This zebrafish study showed that 250 nm polystyrene nanoplastics can act as a Trojan horse by enhancing methylmercury accumulation and directing it toward the head and eyes of larvae over 30 days. Combined exposure worsened behavioral impairment and developmental defects beyond what either contaminant caused alone.
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