Microcystins-Loaded Aged Nanoplastics Provoke a Metabolic Shift in Human Liver Cells

The responseof HepG2 cells upon exposure to microcystins-loadednanoplastics, which was closer to simulate the real scenario thancoexposure (the toxin and nanoplastic) experiments, was mapped. Studiesconcerning the toxicity of pollutant-loaded nanoplastics(NPs) toward humans are still in their infancy. Here, we evaluatedthe adsorption of microcystins (MCs) by pristine and aged polystyrenenanoplastics (PSNPs), prepared MCs-loaded aged PSNPS (1, 5, 10, 15,and 19 & mu;g/mg), and systematically mapped the key molecular changesinduced by aged and MCs-loaded PSNPs to human hepatoblastoma (HepG2)cells. According to the results, MC-LR adsorption is increased 2.64-foldby aging, and PSNP accumulation is detected in HepG2 cells. The cytotoxicityof the MC-LR-loaded aged PSNPs showed a positive relationship withthe MC-LR amount, as the cell viability in the 19 & mu;g/mg loadingtreatment (aPS-MC19) was 10.84% lower than aged PSNPs; meanwhile,more severe oxidative damage was observed. Primary approaches involvedstressing the endoplasmic reticulum and reducing protein synthesisthat the aged PSNPs posed for HepG2 cells, while the aggravated cytotoxicityin aPS-MC19 treatment was a combined result of the metabolic energydisorder, oxidative damage, endoplasmic reticulum stress, and downregulationof the MC-LR target protein. Our results confirm that the aged PSNPscould bring more MC-LR into the HepG2 cells, significantly interferewith biological processes, and provide new insight into decipheringthe risk of NPs to humans.