Mechanism of N-acetyl-cysteine inhibition on the cytotoxicity induced by titanium dioxide nanoparticles in JB6 cells transfected with activator protein-1.

The present study investigated the mechanism of N-acetyl-cysteine (NAC) inhibition on the cytotoxicity induced by titanium dioxide (TiO2) nanoparticles (NPs) using murine epidermal JB6 cells transfected with activator protein-1 (AP-1), JB6-AP-1 cells. Confocal microscopy was performed to localize TiO2 NPs in cultured cells. The level of reactive oxygen species (ROS) present in cells was evaluated by staining with 2',7'-dichlorodihydrofluorescein diacetate and dihydroethidium. AP-1 gene expression levels in the cells were detected using the luciferase assay. Confocal microscopy indicated that TiO2 NPs passed through the cell membrane into the cytoplasm; however, they did not penetrate the nuclear membrane. The present findings indicated that NAC markedly inhibited ROS generation and significantly inhibited cytotoxicity (P<0.05) induced by TiO2 NPs. Furthermore, alternative studies have demonstrated that AP-1 luciferase activity induced by TiO2 NPs may be significantly inhibited by NAC. In conclusion, the ability for NAC to inhibit the cytotoxicity induced by TiO2 NPs may primarily occur by blocking ROS generation in the cultured cells.