Mitochondrial Toxicity of Cadmium Telluride Quantum Dot Nanoparticles in Mammalian Hepatocytes.
Mitochondrial Toxicity of Cadmium Telluride Quantum Dot Nanoparticles in Mammalian Hepatocytes.
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DOI：
10.1093/toxsci/kfv068
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发表时间：
2015-07
期刊：
影响因子：
--
通讯作者：
Willmore WG
中科院分区：
文献类型：
--
作者：
Nguyen KC;Rippstein P;Tayabali AF;Willmore WG
越来越多的研究表明，线粒体是纳米材料诱导毒性的相关靶点。然而，纳米颗粒（NPs）与这些细胞器相互作用并影响其功能的潜在机制尚不清楚。研究碲化镉量子点（CdTe-QD）纳米粒对人肝癌HepG 2细胞线粒体的影响。用透射电镜和共聚焦显微镜观察发现，CdTe-QD处理导致线粒体增大。CdTe量子点似乎与分离的线粒体通过其固有的荧光检测。进一步的分析表明，CdTe-QD引起线粒体膜电位的破坏，增加细胞内钙水平，损害细胞呼吸，并减少腺苷三磷酸合成。量子点对线粒体氧化磷酸化的影响，证明了电子传递链的酶的水平和活性的变化。CdTe-QD处理后过氧化物酶体增殖物激活受体-γ共激活因子水平的升高表明CdTe-QD对线粒体生物合成的影响。我们的研究结果还表明，CdTe-QDs的影响是类似的或更大的氯化镉在等效浓度的镉，这表明，CdTe-QDs的毒性作用并不完全是由于镉从纳米颗粒释放。总体而言，该研究表明，CdTe-QDs通过引起线粒体形态和结构的变化，以及损害其功能和刺激其生物合成来诱导多种毒性。
There are an increasing number of studies indicating that mitochondria are relevant targets in nanomaterial-induced toxicity. However, the underlying mechanisms by which nanoparticles (NPs) interact with these organelles and affect their functions are unknown. The aim of this study was to investigate the effects of cadmium telluride quantum dot (CdTe-QD) NPs on mitochondria in human hepatocellular carcinoma HepG2 cells. CdTe-QD treatment resulted in the enlargement of mitochondria as examined with transmission electron microscopy and confocal microscopy. CdTe-QDs appeared to associate with the isolated mitochondria as detected by their inherent fluorescence. Further analyses revealed that CdTe-QD caused disruption of mitochondrial membrane potential, increased intracellular calcium levels, impaired cellular respiration, and decreased adenosine triphosphate synthesis. The effects of CdTe-QDs on mitochondrial oxidative phosphorylation were evidenced by changes in levels and activities of the enzymes of the electron transport chain. Elevation of peroxisome proliferator-activated receptor-γ coactivator levels after CdTe-QD treatment suggested the effects of CdTe-QDs on mitochondrial biogenesis. Our results also showed that the effects of CdTe-QDs were similar or greater to those of cadmium chloride at equivalent concentrations of cadmium, suggesting that the toxic effects of CdTe-QDs were not solely due to cadmium released from the NPs. Overall, the study demonstrated that CdTe-QDs induced multifarious toxicity by causing changes in mitochondrial morphology and structure, as well as impairing their function and stimulating their biogenesis.
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影响因子：
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