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Effects of long-term exposure of gelatinated and non-gelatinated cadmium telluride quantum dots on differentiated PC12 cells

DOI: 10.1186/1477-3155-10-4

Keywords: CdTe Quantum Dots, Differentiated PC12 cells, Cytotoxicity, Neuronal Growth Factor, Apoptosis

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Abstract:

Long 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.The 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).Quantum Dots (QDs) represent an attractive diagnostic and therapeutic tool, however they possess the major disadvantage of being inherently cytotoxic, due to their cadmium components [1,2]. Cellular interaction with QDs is dependent on a variety of physicochemical parameters, including size, chemical composition, surface structure, solubility, shape and aggregation; all of which can influence or modify cellular uptake [3]. There is an inverse relationship between the size of QDs and their number of surface atoms or molecules that determines the material reactivity, which is the key to defining the chemical and biological properties of QDs [3,4]. The small size of QDs also gives them the ability to traverse cell membranes and possibly the blood-brain barrier, which cannot be achieved using conventional dyes, making their use as therapeutic tools an intriguing possibility. The size of QDs is fundamental to their cellular interaction and has to be considered while studying their toxicity and distribution in various cell compartments [5]. When coated with certain biocompatible polymers, QDs have been shown to be far less toxic to cells and living organisms in the short term [6]. A fundamental problem of QDs is that of aggregation and accumulation, which are particularly prevalent upon entrapment in organelles such as vesicles, endosomes and lysosomes inside living cells [7-9]. However, little information is known about the interactio

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