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

Department of Chemistry, Chung Yuan Christian University, 臺中市, Taiwan, Taiwan
Toxicology Letters (Impact Factor: 3.26). 01/2007; 167(3):191-200. DOI: 10.1016/j.toxlet.2006.09.007
Source: PubMed


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.

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    • "The exposure concentrations we chose in this study based on two reasons. One is that the QDs concentrations used for biological imaging are nano molarities, and the identification of QDs cytotoxicity was also reported at nano molarities by several groups (Duan and Nie 2007; Zhang et al. 2006; Chan et al. 2006), the other reason is that QDs-exposed at 10 nM in our previous studies could elevate intracellular Ca 2? levels and interfere sodium channels functional characteristics (Tang et al. 2008a, b). "
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