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

Department of Bioscience Technology, Center for Nanotechnology, Chung Yuan Christian University, Chung Li, 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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    • "QD toxicity in neural applications is crucial to establish a biocompatible QD-based photoactive neural interface. Toxic effects of QDs include changes in cell morphology, suppressed metabolic activity, and a decrease in cell viability157,158 and are attributed mainly to their composition as well as to their surface coating and nanometer size.159 "
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    • "Cell-based in vitro studies play an essential role in meaningful toxicity testing. Numerous toxi- cological assays have been carried out in order to investigate QD cytotoxicity [14], [15], [16], . Some notable results have been reported regarding the potential cytotoxicity of QDs and related mechanism [18], [19], [20], [21]. "
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    ABSTRACT: With the widespread use of quantum dots (QDs), the likelihood of exposure to quantum dots has increased substantially. The application of quantum dots in numerous biomedical areas requires detailed studies on their toxicity. In this study, we aimed to determine the threshold dose which reduced or eliminated CdTe-induced toxicity in L929 cells by controlling the exposure dose. We established a cellular model of acute exposure to CdTe QDs. Cells were exposed to different concentrations of CdTe QDs (2.2 nm and 3.5 nm) followed by illustrative cytotoxicity analysis. The results showed that low concentrations of CdTe QDs (under 10 µg/mL) promoted cell viability, caused no obvious effect on the rate of cell apoptosis, intracellular calcium levels and changes in mitochondrial membrane potential, while high concentrations significantly inhibited cell viability. In addition, reactive oxygen species in the 10 µg/mL-treated group was significantly reduced compared with the control group. In summary, the cytotoxicity of CdTe QDs on L929 cell is dose-dependent, time-dependent and size-dependent. Low concentrations of CdTe QDs (below 10 µg/mL) may be nontoxic and safe in L929 cells, whereas high concentrations (above 10 µg/mL) may be toxic resulting in inhibition of proliferation and induction of apoptosis in L929 cells.
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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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