Nanoplastics induce more severe apoptosis through mitochondrial damage in Caco-2 cells compared to sub-micron plastics

Abstract Background Small plastic particles such sub-micron- (1μm-100nm) and nanoplastics (<100nm) derived from the environment can enter the human gastrointestinal tract through the food chain. In addition, MPs adsorbed with heavy metals are synergistically toxic to humans. Though the cytotoxicity of different sizes of polystyrene (PS) has been studied, the toxicity study of small sizes PS such as 20 nm on intestinal cells is still utterly limited. Results In the present study, the toxicity of 20 nm and 200 nm PS (PS20, PS200) on Caco-2 cells was investigated. PS20 could disrupt cell membrane integrity at a concentration of 80 μg/mL. The images of laser scanning-confocal illustrated that cell tend to uptake more PS20 than PS200 and those particles were localized in lysosomes and mitochondria. Moreover, the loss of mitochondrial membrane potential of PS20 was more severe than that of PS200, which may account for the significant increase in reactive oxygen species (ROS) levels in the PS20-treated group. Furthermore, PS20 induced cell apoptosis. Moreover, PS enhanced the cytotoxicity of Methylmercury (MeHg). Overall, this study demonstrates that PS had a size- and concentration-dependent cytotoxic effect on the intestine and an enhanced cytotoxic effect on MeHg. Conclusions Both sub-micron and NPs could enter Caco-2 cells. NPS induced apoptosis by inducing mitochondrial damage and was significantly more toxic to cells than sub-micron PS. Both sizes of PS used in the experiments have a synergistic effect on MeHg-induced cytotoxicity. In conclusion, our study demonstrated the strong cytotoxicity of NPs and synergistic toxicity with heavy metals, providing a reference for the environmental toxicity of nanoscale plastics.