详细信息
Oxidative mechanisms contribute to nanosize silican dioxide-induced developmental neurotoxicity in PC12 cells ( SCI-EXPANDED收录)
文献类型:期刊文献
英文题名:Oxidative mechanisms contribute to nanosize silican dioxide-induced developmental neurotoxicity in PC12 cells
作者:Wang, Fen[2];Jiao, Changping[2];Liu, Jianwen[3];Yuan, Huihui[1];Lan, Minbo[1];Gao, Feng[1,2]
机构:[1]E China Univ Sci & Technol, Shanghai Key Lab Funct Mat Chem, Shanghai 200237, Peoples R China;[2]E China Univ Sci & Technol, Dept Pharmaceut, Sch Pharm, Shanghai 200237, Peoples R China;[3]E China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China
年份:2011
卷号:25
期号:8
起止页码:1548
外文期刊名:TOXICOLOGY IN VITRO
收录:;WOS:【SCI-EXPANDED(收录号:WOS:000298362500005)】;
基金:The authors acknowledge 111 program of China (No. B07023) and the financial support from Shanghai nanotechnology leading academic discipline foundation (Nos.0852nm05900 and 0752nm025).
语种:英文
外文关键词:Silica nanoparticles; PC12 cells; Neurotoxicity; Oxidative stress; Apoptosis
摘要:Neurotoxicity was investigated in nano-SiO2-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 SiO2-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-SiO2 exposure (R-2 = 0.965), suggesting the role of oxidative stress on nano-SiO2 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-SiO2 (R-2 = 0.945) suggesting nano-SiO2-induced membrane damage caused by lipid peroxidation. (4) A dose-dependent increase in sub-G1 population in SiO2-exposed cells along with cell shrinkage and nuclear condensation from morphological examination suggesting nano-SiO2-induced cell apoptosis. Furthermore, nano-SiO2 exposure diminished the ability of neurite extension in response to nerve growth factor in treated PC12 cells. In summary, SiO2 nanoparticle exposure resulted in dose-dependent neurotoxicity in cultured PC12 cells that was probably associated with oxidative stress and induced apoptosis. Crown Copyright (C) 2011 Published by Elsevier Ltd. All rights reserved.
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