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• W1971296531 abstract "► An increase ROS level with a decrease in glutathione level suggests nano-SiO 2 -induced free radical generation and glutathione depletion. ► A decrease in cell viability associated with ROS level suggests the role of oxidative stress on nano-SiO 2 induced cell death. ► An increase in thiobarbituric-acid reactive species level suggests nano-SiO 2 -induced membrane damage caused by lipid peroxidation. ► An increase in a cell shrinkage and a nuclear condensation suggesting nano-SiO2-induced cell apoptosis. ► Nano-SiO 2 exposure diminishes the ability of neurite extension in response to NGF in treated PC12 cells. Neurotoxicity was investigated in nano-SiO 2 -treated cultured PC12 cells, an in vitro neuronal cell model, in order to define a relatively safe dose range for its application. The following were observed in the present study: (1) A dose-dependent increase in the level of reactive oxygen species (ROS) with a corresponding decrease in the level of glutathione ( R 2 = 0.965) suggesting 20- and 50-nm SiO 2 -induced free radical generation and glutathione depletion. (2) A dose- and time-dependent decrease in cell viability that was associated with elevation of ROS level, especially after 24-h nano-SiO 2 exposure ( R 2 = 0.965), suggesting the role of oxidative stress on nano-SiO 2 induced cell death. (3) An increase in the level of thiobarbituric-acid reactive species that correlated reversely with cell viability of the PC12 cells treated with nano-SiO 2 ( R 2 = 0.945) suggesting nano-SiO 2 -induced membrane damage caused by lipid peroxidation. (4) A dose-dependent increase in sub-G1 population in SiO 2 -exposed cells along with cell shrinkage and nuclear condensation from morphological examination suggesting nano-SiO 2 -induced cell apoptosis. Furthermore, nano-SiO 2 exposure diminished the ability of neurite extension in response to nerve growth factor in treated PC12 cells. In summary, SiO 2 nanoparticle exposure resulted in dose-dependent neurotoxicity in cultured PC12 cells that was probably associated with oxidative stress and induced apoptosis." @default.
• W1971296531 created "2016-06-24" @default.
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• W1971296531 date "2011-12-01" @default.
• W1971296531 modified "2023-09-24" @default.
• W1971296531 title "Oxidative mechanisms contribute to nanosize silican dioxide-induced developmental neurotoxicity in PC12 cells" @default.
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• W1971296531 doi "https://doi.org/10.1016/j.tiv.2011.05.019" @default.
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