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Nanoplastics as Hepatic Toxicant Vectors: Interactions with Environmental Chemicals, Organelle Dysfunction, and Regulated Cell Death.
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This review summarizes existing research on how tiny nanoplastic particles may affect liver cells. Studies found links between nanoplastic exposure and problems like cell stress, damaged energy-producing structures, and triggered cell death pathways, though results varied depending on the plastic type and test conditions used. The authors note gaps in understanding how these findings relate to real-world health risks.
The environmental accumulation of nanoplastics (NPs) raises concerns regarding their potential effects on hepatic function. Experimental studies suggest that NP exposure can be related with altered mitochondrial electron transport chain activity, reduced ATP availability, changes in Keap1/Nrf2-mediated antioxidant responses, and impaired mitophagy. NPs have also been linked to cytoskeletal alterations, disrupted autophagic flux, and metabolic disturbances that can contribute to processes relevant to metabolic dysfunction-associated steatotic liver disease (MASLD). This review critically evaluates regulated cell death pathways correlated with NP exposure, containing intrinsic apoptosis, RIPK1/RIPK3/MLKL-mediated necroptosis, and NLRP3/cGAS-STING-associated pyroptosis. The available evidence implicates oxidative stress, mitochondrial and lysosomal dysfunction, altered autophagy, metabolic reprogramming, and regulated cell death in nanoplastic-associated hepatic effects. However, mechanistic evidence varies in strength, and observed responses depend on particle composition, surface characteristics, exposure conditions, and experimental models. Particular attention is given to distinguishing associative findings from experimentally supported causal mechanisms and to the limitations of extrapolating results from polystyrene nanoparticle models to other nanoplastics. By integrating evidence on mitochondrial quality control, microRNA-mediated metabolic regulation, and modulated cell death, this review identifies main knowledge gaps relevant to future mechanistic studies and toxicological risk assessment.
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This review examines emerging evidence linking micro- and nanoplastic exposure to liver disease, including metabolic dysfunction-associated liver disease, cirrhosis, and liver cancer. Researchers found that these particles may contribute to liver damage through oxidative stress, inflammation, and disruption of metabolic pathways. The study highlights the need for further research into how environmental plastic contamination may be influencing the rising rates of liver disease worldwide.
Hepatotoxic Mechanisms of Micro- and Nanoplastics in Animal Models: A Scoping Review with Human Health Implications
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This scoping review examines hepatotoxic mechanisms of micro- and nanoplastics in animal models, identifying oxidative stress, inflammation, lipid peroxidation, and epigenetic alterations as the primary pathways through which plastic particles damage liver tissue.
Micro- and nanoplastics induce hepatic injury through organelle stress and fibrotic signaling: mechanisms and therapeutic opportunities
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This review pulls together existing research showing that tiny plastic particles we ingest (from food, water, and packaging) can build up in the liver and damage it from the inside, stressing the cell's internal "power plants" and "recycling centers," triggering inflammation, and eventually causing scarring (fibrosis). This matters because it suggests everyday plastic exposure could contribute to chronic liver disease over time, and the paper points to potential treatments, like antioxidants or therapies targeting gut health, that scientists are exploring to counter this damage.
Impact of microplastics and nanoplastics on liver health: Current understanding and future research directions
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This review summarizes what scientists know about how micro- and nanoplastics affect the liver, which is one of the first organs exposed because it processes everything absorbed from the gut. The particles trigger oxidative stress, disrupt energy metabolism, cause cell death, and promote inflammation, and may contribute to conditions like fatty liver disease and liver fibrosis. The paper also highlights how plastics can disturb the gut microbiome, which communicates with the liver through the gut-liver axis and may amplify liver damage.
Toxicological effects of micro- and nanoplastic exposure reveal resistance mechanisms to programmed cell death in hepatic cells
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This study exposed human liver cells in a lab to tiny plastic particles called microplastics and nanoplastics, including polyethylene and polyethylene terephthalate. The treated cells showed changes in proteins that control cell death, becoming more resistant to dying, including when exposed to a cancer drug.
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