Zhan Qingling, Tang Meng
Key Laboratory of Environmental Medicine and Engineering, Ministry of Education; School of Public Health & Collaborative Innovation Center of Suzhou Nano Science and Technology, Southeast University, Nanjing, 210009, Jiangsu Province, People's Republic of China.
Biol Trace Elem Res. 2014 Oct;161(1):3-12. doi: 10.1007/s12011-014-0068-7. Epub 2014 Jul 27.
Recently, quantum dots (QDs) have been widely applied in biological and biomedical fields such as cell labeling, living tissue imaging, and photodynamic therapy because of their superior optical properties. Meanwhile, the potential biological negative effects and/or toxic effects of QDs have become increasingly important, especially the cytotoxicity caused by QDs. One of the common cytotoxicity when living organisms are treated with QD is apoptosis, where many attempts have been made to explain the mechanisms of apoptosis caused by QDs' use. One of the mechanisms is the production of cadmium ion (Cd(2+)) and reactive oxygen species (ROS). Excess generation of ROS will result in oxidative stress that would mediate apoptosis. Furthermore, the activation of cell death receptors and mitochondria-dependent such as B cell lymphoma 2 (Bcl-2) family and the caspase family could onset apoptosis. Signal transduction such as some classical signal pathways of PI3K-AKT, NF-E2-related factor 2 (Nrf2)-antioxidant response element (ARE), mitogen-activated protein kinases (MAPKs), and nuclear factor kappa B (NF-κB) also plays an important role in the regulation of apoptosis. Several ways to reduce the apoptotic rate have been introduced, such as surface modification, controlling, the dose, size, and exposure time of QDs as well as using antioxidants or inhibitors. In this review, we attempted to review the most recent findings associated with apoptosis caused by QDs so as to provide some guidelines for a safer QD application in the future.
近年来，量子点（QDs）因其优异的光学性质而被广泛应用于生物和生物医学领域，如细胞标记、活组织成像和光动力疗法。与此同时，量子点潜在的生物负面影响和/或毒性作用变得越来越重要，尤其是量子点引起的细胞毒性。生物体用量子点处理时常见的细胞毒性之一是细胞凋亡，人们已经进行了许多尝试来解释量子点使用引起的细胞凋亡机制。其中一个机制是镉离子（Cd(2+)）和活性氧（ROS）的产生。过量产生的ROS会导致氧化应激，进而介导细胞凋亡。此外，细胞死亡受体和线粒体依赖性的激活，如B细胞淋巴瘤2（Bcl-2）家族和半胱天冬酶家族，可能引发细胞凋亡。信号转导，如PI3K-AKT、核因子E2相关因子2（Nrf2）-抗氧化反应元件（ARE）、丝裂原活化蛋白激酶（MAPKs）和核因子κB（NF-κB）等一些经典信号通路，在细胞凋亡的调节中也起着重要作用。已经介绍了几种降低凋亡率的方法，如表面修饰、控制量子点的剂量、大小和暴露时间以及使用抗氧化剂或抑制剂。在这篇综述中，我们试图回顾与量子点引起的细胞凋亡相关的最新发现，以便为未来更安全地应用量子点提供一些指导。
