We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Polystyrene nanoplastics carrying copper ion induce FDX1-mediated cuproptosis
Summary
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.