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Long-Term Exposure to CdTe Quantum Dots Causes Functional Impairments in Live Cells

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    Research Article

    Long-Term Exposure to CdTe Quantum Dots Causes Functional Impairments in Live Cells
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    Department of Pharmacology and Therapeutics, McGill University, Montréal, QC Canada H3G 1Y6, Humboldt-Universität zu Berlin Institut für Physik, AG Photobiophysik, Newtonstrasse 15 D-12489 Berlin, Germany, and Department of Chemistry and Faculty of Pharmacy, Université de Montréal, CP 6128 Succursale Centre Ville, Montréal, QC Canada H3C 3J7
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    Langmuir

    Cite this: Langmuir 2007, 23, 4, 1974–1980
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    https://doi.org/10.1021/la060093j
    Published January 12, 2007
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    Abstract

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    Several studies suggested that the cytotoxic effects of quantum dots (QDs) may be mediated by cadmium ions (Cd2+) released from the QDs cores. The objective of this work was to assess the intracellular Cd2+ concentration in human breast cancer MCF-7 cells treated with cadmium telluride (CdTe) and core/shell cadmium selenide/zinc sulfide (CdSe/ZnS) nanoparticles capped with mercaptopropionic acid (MPA), cysteamine (Cys), or N-acetylcysteine (NAC) conjugated to cysteamine. The Cd2+ concentration determined by a Cd2+-specific cellular assay was below the assay detection limit (<5 nM) in cells treated with CdSe/ZnS QDs, while in cells incubated with CdTe QDs, it ranged from ∼30 to 150 nM, depending on the capping molecule. A cell viability assay revealed that CdSe/ZnS QDs were nontoxic, whereas the CdTe QDs were cytotoxic. However, for the various CdTe QD samples, there was no dose-dependent correlation between cell viability and intracellular [Cd2+], implying that their cytotoxicity cannot be attributed solely to the toxic effect of free Cd2+. Confocal laser scanning microscopy of CdTe QDs-treated cells imaged with organelle-specific dyes revealed significant lysosomal damage attributable to the presence of Cd2+ and of reactive oxygen species (ROS), which can be formed via Cd2+-specific cellular pathways and/or via CdTe-triggered photoxidative processes involving singlet oxygen or electron transfer from excited QDs to oxygen. In summary, CdTe QDs induce cell death via mechanisms involving both Cd2+ and ROS accompanied by lysosomal enlargement and intracellular redistribution.

    Copyright © 2007 American Chemical Society

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    †

     McGill University.

    §

     Université de Montréal.

    ‡

     Humboldt-Universität zu Berlin Institut für Physik.

    *

     Corresponding author. Phone:  (514) 340-5179. Fax:  (514) 340-3245. E-mail:  [email protected].

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