Oxidative mechanisms contribute to nanosize silican dioxide-induced developmental neurotoxicity in PC12 cells

► An increase ROS level with a decrease in glutathione level suggests nano-SiO2-induced free radical generation and glutathione depletion. ► A decrease in cell viability associated with ROS level suggests the role of oxidative stress on nano-SiO2 induced cell death. ► An increase in thiobarbituric-acid reactive species level suggests nano-SiO2-induced membrane damage caused by lipid peroxidation. ► An increase in a cell shrinkage and a nuclear condensation suggesting nano-SiO2-induced cell apoptosis. ► Nano-SiO2 exposure diminishes the ability of neurite extension in response to NGF in treated PC12 cells.