Photoaged polystyrene nanoplastics induce perturbation of glucose metabolism in HepG2 cells via oxidative stress

Micro- & nano-plastics (MNPs) have been considered an emerging persistent pollutant in the environment. Most of the works focus on the potential toxicity of pristine, rather than photoaged, MNPs, let alone the underlying mechanisms of toxicity. To address this gap, we exposed human liver cancer cells (HepG2) to polystyrene nanoplastics (PS-NPs) with varying degrees of photodegradation, including pristine PS-NPs and photoaged PS-NPs irradiated with UV for 8 days (short-term) and 32 days (long-term).The surface characteristics of PS-NPs exhibited a significant alteration as characterized by SEM, FTIR, XPS, and Zetasizer. Exposure to PS-NPs affected cell viability, ion transport capacity and glucose metabolism, and also induced oxidative stress. Photoaged PS-NPs posed relatively higher impacts than pristine ones on HepG2 cells. Long-term photoaged PS-NPs induced the glucose metabolic disorders in a dose-dependent manner, while pristine and short-term photoaged PS-NPs induced the metabolic disorders only at high concentrations. The severe cellular metabolic toxicity of PS-NPs was attributed to the changes in physicochemical properties induced by UV irradiation, such as the production of oxygen-containing functional groups (hydroxyl, carboxyl, and carbonyl groups). Taken together, the long-term photoaged PS-NPs suppressed more than 10 % of cell vitality compared to the pristine ones, and disrupted the glucose metabolism in HepG2 cells, particularly gene expression associated with glucose homeostasis.