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標題: The apoptotic effect of nanosilver is mediated by a ROS- and JNK-dependent mechanism involving the mitochondrial pathway in NIH3T3 cells
作者: Hsin, Y.H.
Chena, C.F.
Huang, S.
Shih, T.S.
Lai, P.S.
Chueh, P.J.
關鍵字: apoptosis;JNK;mitochondria-dependent pathway;nanosilver;reactive;oxygen species;ROS;oxidative stress;cytochrome-c;in-vitro;p53-induced apoptosis;bax;translocation;induce apoptosis;quantum dots;bcl-2;death;p53
Project: Toxicology Letters
期刊/報告no:: Toxicology Letters, Volume 179, Issue 3, Page(s) 130-139.
Nanomaterials and nanoparticles have received considerable attention recently because of their unique properties and diverse biotechnology and life sciences applications. Nanosilver products, which have well-known antimicrobial properties, have been used extensively in a range of medical settings. Despite the widespread use of nanosilver products, relatively few studies have been undertaken to determine the biological effects of nanosilver exposure. The purpose of this study was to evaluate the toxicity of nanosilver and to elucidate possible molecular mechanisms underlying the biological effects of nanosilver. Here, we show that nanosilver is cytotoxic, inducing apoptosis in NIH3T3 fibroblast cells. Treatment with nanosilver induced the release of cytochrome c into the cytosol and translocation of Bax to mitochondria, indicating that nanosilver-mediated apoptosis is mitochondria-dependent. Nanosilver-induced apoptosis was associated with the generation of reactive oxygen species (ROS) and JNK activation, and inhibition of either ROS or JNK attenuated nanosilver-induced apoptosis. In nanosilver-resistant HCT116 cells, upregulation of the anti-apoptotic proteins, Bcl-2 appeared to be associated with a diminished apoptotic response. Taken together, our results provide the first evidence for a molecular mechanism of nanosilver cytotoxicity, showing that nanosilver acts through ROS and JNK to induce apoptosis via the mitochondrial pathway. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
ISSN: 0378-4274
DOI: 10.1016/j.toxlet.2008.04.015
Appears in Collections:化學系所

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