Abstract
BackgroundThe inherent toxicity of unmodified Quantum Dots (QDs) is a major hindrance to their use in biological applications. To make them more potent as neuroprosthetic and neurotherapeutic agents, thioglycolic acid (TGA) capped CdTe QDs, were coated with a gelatine layer and investigated in this study with differentiated pheochromocytoma 12 (PC12) cells. The QD - cell interactions were investigated after incubation periods of up to 17 days by MTT and APOTOX-Glo Triplex assays along with using confocal microscopy.ResultsLong term exposure (up to 17 days) to gelatinated TGA-capped CdTe QDs of PC12 cells in the course of differentiation and after neurites were grown resulted in dramatically reduced cytotoxicity compared to non-gelatinated TGA-capped CdTe QDs.ConclusionThe toxicity mechanism of QDs was identified as caspase-mediated apoptosis as a result of cadmium leaking from the core of QDs. It was therefore concluded that the gelatine capping on the surface of QDs acts as a barrier towards the leaking of toxic ions from the core QDs in the long term (up to 17 days).
Highlights
The inherent toxicity of unmodified Quantum Dots (QDs) is a major hindrance to their use in biological applications
Our aim was to analyze the effect of Cadmium Telluride (CdTe) QDs on cell behaviour and morphology and to investigate any alterations of cell proliferation, cytotoxicity, viability and apoptosis using pre-determined assays
Characterisation of CdTe QDs All types of QDs used in this study were fully characterised prior to their biological testing
Summary
The inherent toxicity of unmodified Quantum Dots (QDs) is a major hindrance to their use in biological applications. The small size of QDs gives them the ability to traverse cell membranes and possibly the blood-brain barrier, which cannot be achieved using conventional dyes, coatings, leading to a leakage of their toxic core particles or ions [8,13]. This core leakage has been shown to initiate the formation of reactive oxygen species (ROS), which are the key mediators in cell organelle damage and destruction. Cytochrome c is released from mitochondrial intermembrane space which activates the downstream caspases 9 and 3, causing cell death by apoptosis [2,14,15,16,17]
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