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Inert polystyrene nanoplastics-induced liver injury in mice was implicated in intense oxidative stress and inflammation mediated by ferroptosis.
Summary
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.