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Polystyrene nanoplastics carrying copper ion induce FDX1-mediated cuproptosis
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Researchers found that polystyrene nanoplastics can act as carriers for copper ions, shuttling them into cells in a "Trojan horse" effect that triggers a recently discovered form of cell death called cuproptosis. Using zebrafish and human liver cells, they showed that combined exposure to nanoplastics and copper disrupted copper balance, damaged mitochondria, and activated cell death pathways. The study identifies a specific protein, FDX1, as a key molecular target in this process, offering new insights into how nanoplastic-metal combinations can be harmful.
Polystyrene nanoplastics (PS-NPs) and copper ions (Cu²⁺) are common environmental pollutants, yet their combined toxicological effects remain poorly understood. This study demonstrates that PS-NPs act as carriers of Cu²⁺, facilitating intracellular accumulation and inducing cuproptosis, a recently identified form of regulated cell death. Using zebrafish larvae and Hep G2 cells, we showed that co-exposure to PS-NPs and Cu²⁺ disrupted copper homeostasis, promoted DLAT oligomerization, impaired mitochondrial structure and function, and activated the cuproptosis pathway. Molecular docking revealed stable binding of PS-NPs and Cu²⁺ to the key regulator FDX1, further aggravating cuproptosis. FDX1 overexpression experiments confirmed its pivotal role, as enhanced expression significantly increased DLAT aggregation and cell death. This study is the first to reveal the molecular mechanism by which PS-NPs mediate FDX1-dependent cuproptosis via a "Trojan horse" effect. These findings provide novel insights into the mechanisms of nanoplastics-heavy metal co-exposure and offer a potential molecular target for mitigating environmental toxicity.
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Polystyrene nanoplastics disrupt iron homeostasis by promoting FPN1 ubiquitination in GC-2spd(ts) cells
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Researchers showed that polystyrene nanoplastics induce ferroptosis — an iron-dependent form of cell death — in mouse sperm precursor cells by promoting the ubiquitin-tagged degradation of the iron-export protein ferroportin1, causing iron to accumulate inside cells, driving lipid peroxidation and mitochondrial damage.
Polystyrene Microplastics Induced Hepatocytes Pyroptosis, Apoptosis and Ferroptosis via GSDMD-N-Mediated Mitochondrial Damage
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Researchers showed that polystyrene microplastics trigger three simultaneous cell death pathways in liver cells — pyroptosis, ferroptosis, and apoptosis — through a cascade where GSDMD-N protein forms pores not only in the plasma membrane but also on mitochondria, amplifying reactive oxygen species and driving lysosomal iron release that initiates ferroptosis.
Combined exposure of polystyrene nanoplastics and silver nanoparticles exacerbating hepatotoxicity in zebrafish mediated by ferroptosis pathway through increased silver accumulation
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When zebrafish were exposed to both polystyrene nanoplastics and silver nanoparticles together, the liver damage was significantly worse than from silver alone because the nanoplastics helped more silver accumulate in the body. The combined exposure triggered a specific type of cell death called ferroptosis in liver tissue, suggesting that nanoplastics can make other environmental pollutants more toxic.
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.
First evidence of CuPANotic cell death in fish gut upon environmentally relevant co-exposure to Copper and PVC microplastics
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Researchers exposed zebrafish to copper and PVC microplastics at environmentally relevant concentrations and found for the first time that the combination triggers CuPANoptosis — a novel cell death pathway integrating cuproptosis and PANoptosis — with PVC increasing gut copper load by 1.6–1.9-fold.
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When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.