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New Sight of Renal Toxicity Caused by UV‐Aged Polystyrene Nanoplastics: Induced Ferroptosis via Adsorption of Transferrin
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Researchers discovered that polystyrene nanoplastics aged by sunlight caused more severe kidney damage in mice than fresh nanoplastics, triggering a type of cell death called ferroptosis. The sun-aged particles grabbed onto a blood protein called transferrin, which carries iron into cells, causing iron overload and cell damage in kidney tissue. This is concerning because most nanoplastics in the real world have been weathered by UV light, meaning they may be more harmful to human kidneys than laboratory studies using fresh plastics suggest.
Secondary nanoplastics (NPs) caused by degradation and aging due to environmental factors are the main source of human exposure, and alterations in the physicochemical and biological properties of NPs induced by environmental factors cannot be overlooked. In this study, pristine polystyrene (PS) NPs to obtain ultraviolet (UV)-aged PS NPs (aPS NPs) as secondary NPs is artificially aged. In a mouse oral exposure model, the nephrotoxicity of PS NPs and aPS NPs is compared, and the results showed that aPS NPs exposure induced more serious destruction of kidney tissue structure and function, along with characteristic changes in ferroptosis. Subsequent in vitro experiments revealed that aPS NPs-induced cell death in human renal tubular epithelial cells involved ferroptosis, which is supported by the use of ferrostatin-1, a ferroptosis inhibitor. Notably, it is discovered that aPS NPs can enhance the binding of serum transferrin (TF) to its receptor on the cell membrane by forming an aPS-TF complex, leading to an increase in intracellular Fe2+ and then exacerbation of oxidative stress and lipid peroxidation, which render cells more sensitive to ferroptosis. These findings indicated that UV irradiation can alter the physicochemical and biological properties of NPs, enhancing their kidney biological toxicity risk by inducing ferroptosis.
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Chronic exposure to polystyrene microplastics induces renal fibrosis via ferroptosis
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Mice exposed to polystyrene microplastics in their drinking water for six months developed kidney scarring (fibrosis) driven by a type of cell death called ferroptosis. The microplastics triggered iron-dependent damage in kidney cells, which then released signals causing surrounding tissue to scar over. This long-term study reveals a new mechanism by which chronic microplastic exposure could lead to progressive kidney disease in humans.
Polystyrene Microplastics Induce Nephrotoxicity via Oxidative Stress, Inflammation, Autophagy, 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.
Inert polystyrene nanoplastics-induced liver injury in mice was implicated in intense oxidative stress and inflammation mediated by ferroptosis.
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Scientists injected mice with nanoplastics (tiny plastic particles similar to those found in our food and water) and found they triggered liver damage through a specific type of cell death linked to iron and oxidative stress, along with signs of kidney stress. While this study used direct injection into mice rather than everyday human exposure, it adds to growing evidence that the nanoplastics we're increasingly exposed to through food and packaging could harm multiple organs, not just the gut where they're first absorbed.
Unraveling the impacts of photolysis-induced aging microplastics on enhanced immunotoxicity and nephrotoxicity
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Researchers compared the toxicity of pristine and sun-aged polyethylene and PET microplastics on kidney cells and immune cells and found that aged particles were up to 40 percent more toxic. The increased harm was attributed to environmentally persistent free radicals that form on plastic surfaces during UV exposure, which amplify oxidative stress inside cells. The study highlights that weathered microplastics in the real environment may pose greater health risks than the pristine particles typically used in laboratory studies.
Co-exposure of arsenic and polystyrene-nanoplastics induced kidney injury by disrupting mitochondrial homeostasis and mtROS-mediated ferritinophagy and ferroptosis
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Researchers found that arsenic and polystyrene nanoplastics together — but not separately — cause kidney fibrosis in mice by disrupting mitochondrial function and triggering a form of iron-dependent cell death called ferroptosis, with mitochondria-targeted antioxidants significantly reducing the combined damage.
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