1 Chemistry Department, College of Science, Princess Nourah Bint Abdulrahman University, Riyadh, Saudi Arabia.
2 Department of Zoology, College of Science, King Saud University, Riyadh, Saudi Arabia.
Hum Exp Toxicol. 2019 Aug;38(8):914-926. doi: 10.1177/0960327119843578. Epub 2019 Apr 17.
Nanotechnology has achieved more commercial attention over recent years, and its application has increased concerns about its discharge in the environment. In this study, we have chosen human hepatic carcinoma (HuH-7) cells because liver tissue has played an important role in human metabolism. Therefore, the objective of this study was to determine DNA damaging and apoptotic potential of cadmium telluride quantum dots (CdTe QDs; average particle size (APS) 10 nm, 1-25 µg/ml) on HuH-7 cells and the basic molecular mechanism of its cellular toxicity. Cytotoxicity of different concentrations of CdTe QDs on HuH-7 cells was determined by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) and lactate dehydrogenase (LDH) tests. Moreover, reactive oxygen species (ROS) generation, mitochondrial membrane potential, DNA damage, and Hoechst 33342 fluorescent staining morphological analysis of necrotic/apoptotic cells were detected; cellular impairment in mitochondria and DNA was confirmed by JC-1 and comet assay, respectively. A dose- and time-dependent cytotoxicity effect of CdTe QDs exposure was observed HuH-7 cells; the significant ( < 0.05) cytotoxicity was found at 25 μg/ml of CdTe QDs exposure. The percentage of cytotoxicity of CdTe QDs (25 μg/ml) in HuH-7 cells reached 62% in 48 h. CdTe QDs elicited intracellular ROS generation and mitochondrial depolarization, and DNA integrity cells collectively advocated the apoptotic cell death at higher concentration. DNA damage was observed in cells due to CdTe QDs exposure, which was mediated by oxidative stress. This study exploring the effects of CdTe QDs in HuH-7 cells has provided valuable insights into the mechanism of toxicity induced by CdTe QDs.
近年来，纳米技术受到了更多的关注，其应用也引起了人们对其在环境中排放的担忧。在本研究中，我们选择人肝癌（HuH-7）细胞，因为肝脏组织在人类新陈代谢中起着重要作用。因此，本研究的目的是确定碲化镉量子点（CdTe QDs；平均粒径（APS）10nm，1-25μg/ml）对 HuH-7 细胞的 DNA 损伤和凋亡潜能及其细胞毒性的基本分子机制。通过 3-（4,5-二甲基噻唑-2-基）-5-（3-羧基甲氧基苯基）-2-（4-磺基苯基）-2H-四唑（MTS）和乳酸脱氢酶（LDH）试验测定不同浓度 CdTe QDs 对 HuH-7 细胞的细胞毒性。此外，检测活性氧（ROS）生成、线粒体膜电位、DNA 损伤和 Hoechst 33342 荧光染色坏死/凋亡细胞形态分析；通过 JC-1 和彗星试验分别证实了细胞线粒体和 DNA 的损伤。观察到 CdTe QDs 暴露对 HuH-7 细胞的剂量和时间依赖性细胞毒性作用；在 25μg/ml 的 CdTe QDs 暴露下，发现了显著的（<0.05）细胞毒性。在 48 小时时，CdTe QDs（25μg/ml）对 HuH-7 细胞的细胞毒性百分比达到 62%。CdTe QDs 引起细胞内 ROS 生成和线粒体去极化，以及 DNA 完整性，这共同表明在更高浓度下发生了凋亡性细胞死亡。由于 CdTe QDs 的暴露，观察到细胞中的 DNA 损伤，这是由氧化应激介导的。本研究探索了 CdTe QDs 在 HuH-7 细胞中的作用，为 CdTe QDs 诱导毒性的机制提供了有价值的见解。
