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陆杰1,2,姚影1,2,汪岩1,2,臧一腾1,2,瞿靖1,2,何克宇1,2,吴添舒1,2,梁雪1,2,魏婷婷1,2,熊丽林1,2,张婷1,2,#,唐萌1,2,*. 碲化镉量子点(CdTe QDs)对肝细胞的毒性效应及线粒体介导的毒性机制研究[J]. 生态毒理学报, 2018, 13(1): 154-162
碲化镉量子点(CdTe QDs)对肝细胞的毒性效应及线粒体介导的毒性机制研究
Study on the Toxicity and Mitochondrial-Mediated Mechanism of Two Hepatocytes Induced by CdTe QDs
投稿时间:2017-07-09  修订日期:2017-08-23
DOI:10.7524/AJE.1673-5897.20170709002
中文关键词:  碲化镉量子点  肝细胞  线粒体损伤  细胞凋亡  活性氧
英文关键词:cadmium telluride quantum dots  hepatocyte  mitochondrial damage  apoptosis  reactive oxygen species
基金项目:国家自然科学基金项目(No.31671034, 81673218, 81473003, 81302461, 81502783, 81573186);国家重大科学研究计划项目(No.2011CB933404)
作者单位
陆杰1,2,姚影1,2,汪岩1,2,臧一腾1,2,瞿靖1,2,何克宇1,2,吴添舒1,2,梁雪1,2,魏婷婷1,2,熊丽林1,2,张婷1,2,#,唐萌1,2,* 1.环境医学工程教育部重点实验室东南大学公共卫生学院苏州纳米科技协同创新中心南京210009 2. 江苏省生物材料与器件重点实验室东南大学南京210009 
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中文摘要:
      本文探讨了碲化镉量子点(CdTe QDs)对肝细胞的毒性效应及其影响因素,为探索量子点的肝毒性机制提供一定依据。采用人肝癌细胞(HepG2)和人正常肝细胞(L02)为细胞模型,设置0、25、50和100 μmol L-1 4个浓度组,采用CCK-8法检测细胞生存率,石墨炉法检测细胞内镉元素含量,采用流式细胞术,装载荧光探针DCFH-DA检测细胞内活性氧水平,采用FITC/PI检测细胞凋亡以及JC-1检测细胞ATP水平。研究结果显示:CdTe QDs诱导2种肝细胞生存率降低,细胞凋亡率升高,细胞对QDs的摄入水平具有时间依赖性,细胞内活性氧水平显著升高,线粒体膜电位降低和ATP含量显著减少,且2种肝细胞比较发现L02细胞损伤程度更为严重。CdTe QDs对2种肝细胞造成损伤,对L02细胞损伤更明显,其原因是L02细胞对CdTe QDs摄取更多,导致进入细胞的QDs引发更为严重的损伤效应。
  
AuthorAffiliation
Lu Jie1,2, Yao Ying1,2, Wang Yan1,2, Zang Yiteng1,2, Qu Jing1,2, He Keyu1,2, Wu Tianshu1,2, Liang Xue1,2, Wei Tingting1,2, Xiong Lilin1,2,Zhang Ting1,2,#, Tang Meng1,2,*1. 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, China 2. Jiangsu Key Laboratory for Biomaterials and Devices; Southeast University, Nanjing 210009, China
英文摘要:
      The aim of this paper was to investigate the hepatotoxicity of cadmium telluride quantum dots (CdTe QDs) and its influencing factors, and provide some basis for exploring the mechanism of liver toxicity of QDs. The human hepatocellular carcinoma (HepG2) and human normal hepatocytes (L02) were considered as the cell models. The cell viability was measured by CCK-8 method after cells were treated with CdTe QDs at 0, 25, 50 and 100 μmol L-1. The content of cadmium in the cells was measured by graphite furnace method. The intracellular reactive oxygen species (ROS) were measured by DCFH-DA assay. The level of ATP was detected through JC-1 method. Apoptosis was detected by Annexin V-FITC/PI-FCM assay. The CCK-8 results showed that CdTe QDs inhibited the proliferation of HepG2 and L02 cells in a concentration- and time-dependent manner. Meanwhile, the apoptosis rate was obviously increased compared with the control (P<0.05). The uptakes of CdTe QDs by both hepatocytes were also in a time-dependent manner. The levels of intracellular reactive oxygen species were significantly increased. The mitochondrial membrane potential and ATP content in QDs-treated cells decreased significantly compared to the control, which suggested the mitochondrial damage. Taking into account all the findings, it was concluded that the L02 cells were damaged more seriously by CdTe QDs. CdTe QDs caused damage to both liver cells, and more importantly, the L02 cell damage induced by CdTe QDs is more serious than that of HepG2 cells, possibly because L02 cells prefer to intake more QDs, resulting in more serious detrimental effect.
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