论文部分内容阅读
目的研究卷烟烟气凝集物(cigarette smoke condensate,CSC)对人乳头状病毒永生化的人支气管上皮细胞(human papillomavirus-immortalized human bronchial epithelial cell line,BEP2D)线粒体的氧化损伤。方法采用分子探针2’,7’-二氯荧光黄双乙酸盐(2’,7’-dichlorofluorescein diacetate,DCFH-DA)和氢化乙啶(hydroethidine,HE)检测细胞内活性氧(reactive oxygen species,ROS)水平;用荧光标记物MCB(Monochlorobimane)、壬基吖啶橙(nonyl acridine orange,NAO)、四氯四乙基苯并咪唑基羰花青碘化物(5,5’,6,6’-tetrachloro-1,1’,3,3’-tetrethyl benzimidalyl carbocyanine iodide,JC-1)检测细胞内还原型谷胱甘肽(glutathione,GSH)及线粒体内膜心磷脂(cardiolipin,CL)、膜电位(mitochondrial membrane poten-tial,Δψm)。结果CSC作用BEP2D细胞后,细胞内ROS显著增加,GSH及线粒体CL、Δψm水平明显下降,并呈现较好的剂量效应关系。结论CSC可造成细胞线粒体氧化损伤。
Objective To investigate the oxidative damage of human papillomavirus-immortalized human bronchial epithelial cell line (BEP2D) mitochondria by cigarette smoke condensate (CSC). Methods The intracellular reactive oxygen species (ROS) were detected by molecular probe 2 ’, 7’-dichlorofluorescein diacetate (DCFH-DA) and hydroethidine (HE) (5), 6 ’, 6’, 6 ’, 6’, 6 ’, 6’-dithiocarbamate Tetrathyl benzimidyl carbocyanine iodide (JC-1) was used to detect intracellular glutathione (GSH) and mitochondrial membrane endocardial cardiolipin (CL), membrane potential (mitochondrial membrane poten-tial, Δψm). Results After CSC treated with BEP2D cells, intracellular ROS increased significantly, GSH and mitochondrial CL, Δψm levels decreased significantly, and showed a good dose-response relationship. Conclusion CSC can cause mitochondrial oxidative damage.