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Nephrotoxicity induced by PLA NPs and CuSO4: Crosstalk between Cu metabolism and ferroptosis via ATP7B autophagy.
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Researchers exposed mice to polylactic acid nanoplastics and copper sulfate together and found that the nanoplastics triggered autophagy-mediated degradation of the copper transporter ATP7B in kidney cells, causing copper overload that activated ferroptosis and structural glomerular damage—a previously unknown link between biodegradable nanoplastics and metal-induced kidney injury.
Polylactic acid (PLA) plastics exhibit greater environmental degradability than petroleum-based plastics, potentially exacerbating nanoplastic (NPs) formation that enters the food chain. PLA NPs can accumulate in kidneys and transport heavy metals like copper (Cu) due to their high surface area and charge properties. Ferroptosis, an iron-dependent cell death pathway, is implicated in renal diseases. While Cu homeostasis disruption may interact with ferroptosis. This study explored PLA NPs and Cu-induced kidney injury, examining Cu-ferroptosis crosstalk and autophagy's regulatory role. Our findings demonstrated that PLA NPs and copper sulfate (CuSO) co-exposure induced structural and functional damage in the mouse kidney, especially specific changes in the glomerular filtration barrier, accompanied by Cu overload, oxidative stress and ferroptosis activation. Ferrostatin-1 inhibitor markedly attenuated these effects. Mechanistically, autophagy-mediated degradation of the Cu transporter ATP7B plays a crucial role in promoting Cu accumulation and subsequent ferroptosis. This study not only reveals a novel link between PLA NPs exposure and Cu-induced nephrotoxicity but also provides therapeutic targets for mitigating kidney injury caused by biodegradable plastics and metal overload, laying the groundwork for the interplay between Cu metabolism and ferroptosis.
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Researchers reviewed the mechanisms by which polystyrene microplastics damage kidney tissue, finding that they converge on oxidative stress, NF-κB/NLRP3 inflammatory activation, and disruption of autophagy and ferroptosis pathways, with hub genes TP53 and TNF central to the toxic network and particle aging amplifying toxicity.
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