Liver Toxicity of Cadmium Telluride Quantum Dots (CdTe QDs) Due to Oxidative Stress in Vitro and in Vivo.
Liver Toxicity of Cadmium Telluride Quantum Dots (CdTe QDs) Due to Oxidative Stress in Vitro and in Vivo.
复制标题
碲化镉量子点 (CdTe QD) 因体外和体内氧化应激而产生的肝脏毒性
DOI：
10.3390/ijms161023279
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发表时间：
2015-09-25
影响因子：
5.6
通讯作者：
Pu Y
中科院分区：
文献类型：
--
作者：
Zhang T;Hu Y;Tang M;Kong L;Ying J;Wu T;Xue Y;Pu Y
随着量子点应用领域的不断扩大，许多研究报道了量子点潜在的不良反应，但对量子点在肝脏中的潜在毒性研究较少。本研究的目的是研究碲化镉（CdTe）量子点在小鼠和小鼠肝癌细胞α小鼠肝12（AML 12）的影响。碲化镉量子点管理显着增加脂质过氧化物标记丙二醛（MDA）在治疗小鼠的肝脏中的水平。此外，CdTe量子点引起的细胞毒性在AML 12细胞中的剂量和时间依赖性的方式，这可能是通过产生活性氧（ROS）和诱导细胞凋亡介导的。ROS生成的增加伴随着肿瘤抑制基因p53、促凋亡基因Bcl-2的基因表达的增加和抗凋亡基因Bax的减少，表明线粒体介导的途径参与了CdTe QDs诱导的细胞凋亡。最后，我们发现，NF-E2相关因子2（Nrf 2）的缺陷阻断诱导的氧化应激，以保护细胞免受损伤的CdTe量子点。这些研究结果提供了深入了解参与激活Nrf 2信号，赋予对碲化镉量子点诱导的肝细胞凋亡的保护机制。
With the applications of quantum dots (QDs) expanding, many studies have described the potential adverse effects of QDs, yet little attention has been paid to potential toxicity of QDs in the liver. The aim of this study was to investigate the effects of cadmium telluride (CdTe) QDs in mice and murine hepatoma cells alpha mouse liver 12 (AML 12). CdTe QDs administration significantly increased the level of lipid peroxides marker malondialdehyde (MDA) in the livers of treated mice. Furthermore, CdTe QDs caused cytotoxicity in AML 12 cells in a dose- and time-dependent manner, which was likely mediated through the generation of reactive oxygen species (ROS) and the induction of apoptosis. An increase in ROS generation with a concomitant increase in the gene expression of the tumor suppressor gene p53, the pro-apoptotic gene Bcl-2 and a decrease in the anti-apoptosis gene Bax, suggested that a mitochondria mediated pathway was involved in CdTe QDs’ induced apoptosis. Finally, we showed that NF-E2-related factor 2 (Nrf2) deficiency blocked induced oxidative stress to protect cells from injury induced by CdTe QDs. These findings provide insights into the regulatory mechanisms involved in the activation of Nrf2 signaling that confers protection against CdTe QDs-induced apoptosis in hepatocytes.