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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.
Polystyrene nanoplastics (PS-NPs) are emerging food safety contaminants. Ferroptosis is iron-dependent cell death, but its role in PS-NPs hepatotoxicity is unclear. Mice received tail-vein injection of PS-NPs (2-8mg/kg). PS-NPs caused liver injury (elevated transaminases) and possible renal impairment (increased uric acid/creatinine/urea). Hepatic GSH and SOD decreased, IL-1β and TNF-α increased. Mitochondrial shrinkage and cristae loss (ferroptotic features) were observed. PS-NPs upregulated ACSL4, MDA, 4-HNE and TfR, but suppressed FTH1, FPN1, SLC7A11 and GPx4. Thus, ferroptosis mediates PS-NPs liver injury with oxidative stress and inflammation, and PS-NPs may exert multi-organ toxicity.
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Ferroptosis participated in inhaled polystyrene nanoplastics-induced liver injury and fibrosis
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Mice that inhaled polystyrene nanoplastics for up to 12 weeks developed liver injury and scarring (fibrosis), with damage worsening over time and at higher doses. The nanoplastics triggered a specific type of cell death called ferroptosis, which involves iron-dependent damage to cell membranes in the liver. This is one of the first studies to show that breathing in nanoplastics can cause serious liver damage, raising concerns about long-term health effects from airborne plastic pollution.
Activation of pyroptosis and ferroptosis is involved in the hepatotoxicity induced by polystyrene microplastics in mice
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Researchers exposed mice to polystyrene microplastics and found that the particles caused significant liver damage, including structural changes and impaired function. The study identified two specific cell death pathways, pyroptosis and ferroptosis, as key mechanisms driving the liver injury. These findings suggest that microplastic exposure may harm liver health through multiple biological pathways that warrant further investigation.
Polystyrene nanoplastics trigger ferroptosis-dependent liver injury caused by ACSL4 overaccumulation.
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In liver cells and mice, exposure to polystyrene nanoplastics caused liver damage linked to a cell death process called ferroptosis. The plastics disrupted lysosomes, cell structures involved in breaking down materials, leading to buildup of a protein called ACSL4 that drove this damage.
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.
The mechanism of vascular injury caused by polystyrene microplastics: Involving ferroptosis and metabolomics
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Mice exposed to microplastics showed damaged blood vessels, worse cholesterol levels, and a type of cell death called ferroptosis (basically cells dying from oxidative damage). A drug that blocked this cell death reduced the vessel damage, hinting that microplastics may harm heart and blood vessel health, though this was shown in mice, not yet confirmed in humans.
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