National Centre for Biomedical Engineering Science, National University of Ireland Galway, Galway, Ireland.
J Nanobiotechnology. 2012 Jan 20;10:4. doi: 10.1186/1477-3155-10-4.
The 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.
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).
未经修饰的量子点(Quantum Dots,QDs)的固有毒性是其在生物应用中的主要障碍。为了提高它们作为神经修复和神经治疗剂的效果,本研究用巯基乙酸(thioglycolic acid,TGA)包覆的 CdTe QDs 进行了包覆,并对其进行了研究。通过 MTT 和 APOTOX-Glo Triplex 测定以及共聚焦显微镜观察,研究了长达 17 天的培养期内 QD 与细胞的相互作用。
在分化过程中和神经突生长后,PC12 细胞长期(长达 17 天)暴露于胶态 TGA 包覆的 CdTe QDs 中,与非胶态 TGA 包覆的 CdTe QDs 相比,细胞毒性显著降低。
QD 的毒性机制被确定为半胱天冬酶介导的细胞凋亡,这是由于 Cd 从 QD 的核心中泄漏所致。因此可以得出结论,在长期(长达 17 天)内,QD 表面的明胶包覆起到了阻止核心 QD 中有毒离子泄漏的作用。