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The size-dependence and reversibility of polystyrene nanoplastics-induced lipid accumulation in mice: Possible roles of lysosomes
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This mouse study found that smaller nanoplastics (100 nm) cause more fat buildup in the liver than larger ones (500 nm), showing that size matters when it comes to health effects. Encouragingly, the liver damage was reversible after the mice stopped being exposed, suggesting the body can recover once nanoplastic intake is reduced. The damage appears to work by disrupting the cell's waste-recycling system (lysosomes).
Nanoplastics (NPs) continue to accumulate in global aquatic and terrestrial systems, posing a potential threat to human health through the food chain and/or other pathways. Both in vivo and in vitro studies have confirmed that the liver is one of the main organs targeted for the accumulation of NPs in living organisms. However, whether exposure to NPs induces size-dependent disorders of liver lipid metabolism remains controversial, and the reversibility of NPs-induced hepatotoxicity is largely unknown. In this study, the effects of long-term exposure to environmentally relevant doses of polystyrene nanoplastics (PS-NPs) on lipid accumulation were investigated in terms of autophagy and lysosomal mechanisms. The findings indicated that hepatic lipid accumulation was more pronounced in mice exposed to 100 nm PS-NPs compared to 500 nm PS-NPs. This effect was effectively alleviated after 50 days of self-recovery for 100 nm and 500 nm PS-NPs exposure. Mechanistically, although PS-NPs exposure activated autophagosome formation through ERK (mitogen-activated protein kinase 1)/mTOR (mechanistic target of rapamycin kinase) signaling pathway, the inhibition of Rab7 (RAB7, member RAS oncogene family), CTSB (cathepsin B), and CTSD (cathepsin D) expression impaired lysosomal function, thereby blocking autophagic flux and contributing to hepatic lipid accumulation. After termination of PS-NPs exposure, lysosomal exocytosis was responsible for the clearance of PS-NPs accumulated in lysosomes. Furthermore, impaired lysosomal function and autophagic flux inhibition were effectively alleviated. This might be the main reason for the alleviation of PS-NPs-induced lipid accumulation after recovery. Collectively, we demonstrate for the first time that lysosomes play a dual role in the persistence and reversibility of hepatotoxicity induced by environmental relevant doses of NPs, which provide novel evidence for the prevention and intervention of liver injury associated with nanoplastics exposure.
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Researchers exposed mouse and human liver cells and live mice to polystyrene nanoplastics of five different sizes and found that the smallest particles were most toxic in lab dishes, while medium and large particles caused the most liver damage in living animals. The larger particles triggered immune responses by recruiting inflammatory cells to the liver and intestines, causing tissue damage. This study reveals that nanoplastic size matters in unexpected ways, and that lab tests alone may not predict which particles are most dangerous in the body.
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Researchers compared how micro-sized and nano-sized polystyrene plastic particles affect fat metabolism in zebrafish liver cells. They found that both sizes were taken up by cells, but the smaller nanoplastics caused more pronounced disruptions to lipid profiles and triggered cell death pathways. The findings underscore that particle size matters when assessing the biological impact of plastic pollution on fish.
The size-dependence and reversibility of polystyrene nanoplastics-induced hepatic pyroptosis in mice through TXNIP/NLRP3/GSDMD pathway
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Researchers exposed mice to environmentally relevant doses of polystyrene nanoplastics of two different sizes and found that both triggered inflammatory cell death in liver tissue. The smaller particles (100 nm) caused more severe effects than the larger ones (500 nm), working through a specific inflammatory pathway. Importantly, the study found that this liver damage was reversible after exposure stopped, with inflammation returning to near-normal levels after a 50-day recovery period.
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ReversibilityofRenal Fibrosis Induced by Exposureto Polystyrene Nanoplastics: The Dual Role of Lysosomes
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This mouse study investigated whether kidney fibrosis caused by low-level polystyrene nanoplastics (100 nm and 500 nm) is reversible, finding that 100 nm particles caused more severe fibrosis and that lysosomes played a dual role — initially impairing autophagy flux to promote fibrosis, then recovering to facilitate partial reversal after exposure ended.
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