Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University and Jiangsu Key Laboratory for Biomaterials and Devices, Southeast University, Nanjing, 210009, China.
Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University and Jiangsu Key Laboratory for Biomaterials and Devices, Southeast University, Nanjing, 210009, China.
Environ Pollut. 2021 Apr 1;274:115681. doi: 10.1016/j.envpol.2020.115681. Epub 2020 Oct 5.
Quantum dots (QDs) are nanoparticles of inorganic semiconductors and have great promise in various applications. Many studies have indicated that mitochondria are the main organelles for the distribution and toxic effects of QDs. However, the underlying mechanism of QDs interacting with mitochondria and affecting their function is unknown. Here, we report the mechanism of toxic effects of 3-mercaptopropionic acid (MPA)-capped CdTe QDs on mitochondria. Human liver carcinoma (HepG2) cells were exposed to 25, 50 and 100 μmol/L of MPA-capped CdTe QDs. The results indicated that MPA-capped CdTe QDs inhibited HepG2 cell proliferation and increased the extracellular release of LDH in a concentration-dependent manner. Furthermore, MPA-capped CdTe QDs caused reactive oxygen species (ROS) generation and cell damage through intrinsic apoptotic pathway. MPA-capped CdTe QDs can also lead to the destruction of mitochondrial cristae, elevation of intracellular Ca levels, decreased mitochondrial transmembrane potential and ATP production. Finally, we showed that MPA-capped CdTe QDs inhibited mitochondrial fission, mitochondrial inner membrane fusion and mitophagy. Taken together, MPA-capped CdTe QDs induced significant mitochondrial dysfunction, which may be caused by imbalanced mitochondrial fission/fusion and mitophagy inhibition. These findings provide insights into the regulatory mechanisms involved in MPA-capped CdTe QDs-induced mitochondrial dysfunction.
量子点（QDs）是无机半导体的纳米粒子，在各种应用中具有很大的前景。许多研究表明，线粒体是 QDs 分布和毒性作用的主要细胞器。然而，QDs 与线粒体相互作用并影响其功能的潜在机制尚不清楚。在这里，我们报告了 3-巯基丙酸（MPA）封端的 CdTe QDs 对线粒体的毒性作用机制。将人肝癌（HepG2）细胞暴露于 25、50 和 100 μmol/L 的 MPA 封端的 CdTe QDs。结果表明，MPA 封端的 CdTe QDs 以浓度依赖的方式抑制 HepG2 细胞增殖并增加细胞外 LDH 的释放。此外，MPA 封端的 CdTe QDs 通过内在凋亡途径引起活性氧（ROS）的产生和细胞损伤。MPA 封端的 CdTe QDs 还可以导致线粒体嵴的破坏、细胞内 Ca 水平升高、线粒体跨膜电位和 ATP 产生减少。最后，我们表明 MPA 封端的 CdTe QDs 抑制线粒体分裂、线粒体内膜融合和自噬。总之，MPA 封端的 CdTe QDs 诱导明显的线粒体功能障碍，这可能是由于线粒体分裂/融合和自噬抑制的失衡所致。这些发现为 MPA 封端的 CdTe QDs 诱导的线粒体功能障碍的调节机制提供了深入了解。
