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Microcystins-Loaded Aged Nanoplastics Provoke a Metabolic Shift in Human Liver Cells
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Researchers found that aged polystyrene nanoplastics can adsorb significantly more microcystin toxins than pristine nanoplastics, and the toxin-loaded particles caused greater harm to human liver cells. The combined exposure triggered metabolic energy disruption, oxidative damage, and stress in cellular machinery. The study suggests that environmentally weathered nanoplastics may pose amplified health risks by carrying higher loads of harmful waterborne toxins.
Studies concerning the toxicity of pollutant-loaded nanoplastics (NPs) toward humans are still in their infancy. Here, we evaluated the adsorption of microcystins (MCs) by pristine and aged polystyrene nanoplastics (PSNPs), prepared MCs-loaded aged PSNPS (1, 5, 10, 15, and 19 μg/mg), and systematically mapped the key molecular changes induced by aged and MCs-loaded PSNPs to human hepatoblastoma (HepG2) cells. According to the results, MC-LR adsorption is increased 2.64-fold by aging, and PSNP accumulation is detected in HepG2 cells. The cytotoxicity of the MC-LR-loaded aged PSNPs showed a positive relationship with the MC-LR amount, as the cell viability in the 19 μg/mg loading treatment (aPS-MC19) was 10.84% lower than aged PSNPs; meanwhile, more severe oxidative damage was observed. Primary approaches involved stressing the endoplasmic reticulum and reducing protein synthesis that the aged PSNPs posed for HepG2 cells, while the aggravated cytotoxicity in aPS-MC19 treatment was a combined result of the metabolic energy disorder, oxidative damage, endoplasmic reticulum stress, and downregulation of the MC-LR target protein. Our results confirm that the aged PSNPs could bring more MC-LR into the HepG2 cells, significantly interfere with biological processes, and provide new insight into deciphering the risk of NPs to humans.
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Photoaged polystyrene nanoplastics induce perturbation of glucose metabolism in HepG2 cells via oxidative stress
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Researchers exposed human liver cells to polystyrene nanoplastics with varying degrees of UV-induced aging and found that photoaged particles caused more severe disruptions to glucose metabolism than pristine ones. Long-term photoaged nanoplastics triggered dose-dependent metabolic disorders through oxidative stress, while pristine particles only caused effects at high concentrations. The study suggests that weathered nanoplastics in the environment may pose greater health risks than fresh plastic particles.
The presence of polystyrene nanoplastics enhances the MCLR uptake in zebrafish leading to the exacerbation of oxidative liver damage
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Researchers found that polystyrene nanoplastics enhanced the uptake of the toxin microcystin-LR in zebrafish liver over three months of co-exposure, exacerbating oxidative damage and cellular swelling compared to microcystin exposure alone.
Aged fragmented-polypropylene microplastics induced ageing statues-dependent bioenergetic imbalance and reductive stress: In vivo and liver organoids-based in vitro study
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Researchers tested UV-aged polypropylene microplastics from everyday plastic cup lids on mice and lab-grown liver tissue, finding that more heavily aged particles caused greater liver damage. The aged microplastics disrupted energy production in liver cells and caused a harmful buildup of antioxidant molecules, suggesting that the weathered microplastics people encounter in daily life may be more toxic than pristine ones.
Hepatotoxic of polystyrene microplastics in aged mice: Focus on the role of gastrointestinal transformation and AMPK/FoxO pathway
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This study found that polystyrene microplastics caused liver damage in aged mice, with the particles undergoing chemical changes as they passed through the digestive system that may have made them more harmful. The microplastics disrupted key metabolic pathways in the liver, triggered inflammation, and caused DNA damage through oxidative stress. The findings are especially concerning because older individuals may be more vulnerable to the liver-damaging effects of microplastic exposure.
Butylparaben-Loaded Aged Polystyrene Nanoplastics Amplify Its Toxicity in Microcystis aeruginosa via Quorum Sensing Suppression and Enhanced Microcystin-LR Release
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Researchers found that aged nanoplastics (those weathered by the environment) are much better at absorbing and carrying the chemical butylparaben into harmful algae called Microcystis aeruginosa. The contaminated nanoplastics caused the algae to release more of a dangerous toxin called microcystin-LR, which can contaminate drinking water. This study shows how nanoplastics can amplify the harmful effects of other pollutants in water systems that supply human drinking water.
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