CdSe quantum dots induce apoptosis in human neuroblastoma cells via mitochondrial-dependent pathways and inhibition of survival signals
CdSe quantum dots induce apoptosis in human neuroblastoma cells via mitochondrial-dependent pathways and inhibition of survival signals
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DOI：
10.1016/j.toxlet.2006.09.007
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发表时间：
2006-12-15
影响因子：
3.5
通讯作者：
Lu, Pin-Zhen
中科院分区：
文献类型：
--
作者：
Chan, Wen-Hsiung;Shiao, Nion-Heng;Lu, Pin-Zhen
量子点（QDs）可能是一种有用的新型发光标记，但其细胞毒性尚未得到充分研究。在本报告中，我们证明了CdSe-core QDs可以在IMR-32人神经母细胞瘤细胞系中诱导凋亡的生化变化，包括JNK激活、线粒体膜电位丧失、线粒体细胞色素c释放和caspase-9和caspase-3的激活。重要的是，用CdSe-core QD处理IMR-32细胞会引发活性氧（ROS）的增加，并抑制生存相关的信号事件，如Ras和Raf-1蛋白表达的降低以及ERK激活的降低。这些凋亡的生化变化在用zns包被CdSe量子点处理的细胞中未被检测到。综上所述，这些结果表明，CdSe-core QD处理IMR-32细胞诱导JNK活化和线粒体依赖性凋亡过程，同时抑制Ras -> ERK存活信号，ZnS涂层可以有效降低QD的细胞毒性。2006爱思唯尔爱尔兰有限公司版权所有。
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.