Abstract
Toxicity of arsenic (As) has been widely characterized. However, few studies focus on whether cell responses induced by As at nontoxic concentration could be inherited and further change cell tolerance to another pollutant. In this study, human A549 and HeLa cells were exposed to As at nontoxic concentrations for 10 or 15 passages, then the cells were recovered in the cell medium without As. At 25th passage, residual As in both type of cells was completely removed through the recovery process. And no abnormity in cell viability was identified in both type of cells between control and As-treated groups. Above results indicated that As exposure-recovery treatment had limited influence on phenotype of the cells. However, gene expression profiles determined by high-throughput sequencing showed that As exposure-recovery treatment induced similar expression modification of genes related to inflammation, oxidative stress and epigenetic modulation in the A549 and HeLa cells after recovery of 10 or 15 passages, indicating that As-induced cellular responses have been partially memorized at transcriptional level. The memory effect might play key roles in increased tolerance of the A549 and HeLa cells to adverse effects (cell viability, intracellular reactive oxygen species (ROS) generation and plasma membrane damage) induced by titanium dioxide nanoparticles (as representative pollutant). This study shed new lights on toxic effects induced by As at nontoxic concentration, which is useful for risk assessment of combined effects of As and other pollutants.