PS and As jointly induced ROS and DNA damage to activate the apoptotic pathway.
•
PS promoted the accumulation of As in AGS cells.
•
PS aggravated the toxicity of As by disturbing ABC transporter and cytoskeleton.
•
Small-sized PS had a stronger effect on the toxicity of As than the large-sized PS.
Abstract
The coexistence of nanoplastics (NPs) and pollutants such as arsenic (As) has become an unignorable environmental problem. However, there is still a considerable knowledge gap about the impact of NPs and pollutants on human health risks. In this study, the human gastric adenocarcinoma (AGS) cells were used as a model to investigate the toxicity of NPs with different particle sizes and As by MTT assay, western blotting, immunofluorescence and so on. The results showed that 20 nm (8 μg/mL), 50 nm (128 μg/mL), 200 nm (128 μg/mL), 500 nm (128 μg/mL), 1000 nm (128 μg/mL) polystyrene (PS) did not affect cell viability, ROS, intracellular calcium and activate apoptosis pathway in AGS cells. However, noncytotoxic concentration of NPs enhanced the cytotoxicity and intracellular accumulation of As. NPs destroys the fluidity of cell membrane and cytoskeleton, inhibits the activity of ABC transporter, and leads to the accumulation of As in cells. This work highlights that the damage caused by NPs, especially at the level of noncytotoxicity, joint with As cannot be ignored and provides a specific toxicological mechanism of NPs accompanied by exposure to As.
