CdSe quantum dots induce apoptosis in human neuroblastoma cells via mitochondrial-dependent pathways and inhibition of survival signals

被引:224
作者
Chan, Wen-Hsiung
Shiao, Nion-Heng
Lu, Pin-Zhen
机构
[1] Chung Yuan Christian Univ, Ctr Nanotechnol, Dept Biosci Technol, Chungli 32023, Taiwan
[2] Chung Yuan Christian Univ, Dept Chem, Chungli 32023, Taiwan
关键词
quantum dot; apoptosis; JNK; ERK; ROS;
D O I
10.1016/j.toxlet.2006.09.007
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
Quantum dots (QDs) may be useful as novel luminescent markers, but their cytotoxicity has not been fully investigated. In this report, we demonstrate that CdSe-core QDs can induce apoptotic biochemical changes, including JNK activation, loss of mitochondrial membrane potential, mitochondrial release of cytochrome c and activation of caspase-9 and caspase-3 in the IMR-32 human neuroblastoma cell line. Importantly, treatment of IMR-32 cells with CdSe-core QD triggered an increase in reactive oxygen species (ROS) and inhibited survival-related signaling events, such as decreased Ras and Raf-1 protein expression and decreased ERK activation. These apoptotic biochemical changes were not detected in cells treated with ZnS-coated CdSe QDs. Collectively, these results demonstrate that CdSe-core QD treatment of IMR-32 cells induced JNK activation and mitochondrial-dependent apoptotic processes while inhibiting Ras -> ERK survival signaling and that a ZnS coating could effectively reduce QD cytotoxicity. (c) 2006 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:191 / 200
页数:10
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