卷烟烟气对细胞线粒体氧化损伤的研究

米娜; 杨陟华; 潘秀颉; 曹珍山; 陈忠民; 刘刚; 魏菡; 李慧颖; 朱茂祥

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卷烟烟气对细胞线粒体氧化损伤的研究

论著 | 更新时间：2026-01-09

- 卷烟烟气对细胞线粒体氧化损伤的研究
- Oxidative damage of cellular mitochondria by cigarette smoke
- 陆军军医大学学报 2008年30卷第3期页码：257-259
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  中图分类号： R163;R322.34;R329.25
- 纸质出版：2008
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米娜,杨陟华,潘秀颉,曹珍山,陈忠民,刘刚,魏菡,李慧颖,朱茂祥.卷烟烟气对细胞线粒体氧化损伤的研究[J].陆军军医大学学报(原第三军医大学学报),2008,30(03):257-259.

　MI Na,YANG Zhi-hua,PAN Xiu-jie,CAO Zhen-shan,CHEN Zhong-min,LIU Gang,WEI Han,LI Hui-ying,ZHU Mao-xiang.Oxidative damage of cellular mitochondria by cigarette smoke[J].J Amry Med Univ (J Third Mil Med Univ),2008,30(03):257-259.
米娜,杨陟华,潘秀颉,曹珍山,陈忠民,刘刚,魏菡,李慧颖,朱茂祥.卷烟烟气对细胞线粒体氧化损伤的研究[J].陆军军医大学学报(原第三军医大学学报),2008,30(03):257-259. DOI：

　MI Na,YANG Zhi-hua,PAN Xiu-jie,CAO Zhen-shan,CHEN Zhong-min,LIU Gang,WEI Han,LI Hui-ying,ZHU Mao-xiang.Oxidative damage of cellular mitochondria by cigarette smoke[J].J Amry Med Univ (J Third Mil Med Univ),2008,30(03):257-259. DOI：

摘要

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’-tetrachloro-1

1’

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 potential，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。

Abstract

Objective To investigate oxidative damage of mitochondria by cigarette smoke condensate (CSC) in immortalized human bronchial epithelial cells (BEP2D). Methods BEP2D cells were treated with 0

20 μg/ml CSC respectively. 2’

7’-dichlorofluorescein (DCF) and ehidium bromide (EB)

the fluorescent products of the membrane-permeable dyes [2’

7’-dichlorofluorescein diacetate (DCFH-DA) and Hydroethidine (HE)] were used to monitor the intracellular production of reactive oxygen species (ROS) by Fluroskan Ascent FL. The cells were labeled by fluorescent dyes (Monochlorobimane

nonyl acridine orange or 5

5’

6’-tetrachloro-1

1’

3’-tetrethyl benzimidalyl carbocyanine iodide respectively) and then intracellular reduced glutathione (GSH) and mitochondrial cardiolipin

mitochondrial membrane potential were determined by monitoring the fluorescence intensity. Results The ROS production in CSC treated BEP2D cells increased remarkably

and the level of GSH

cardiolipin and membrane potential decreased obviously

both in a good dose-effect relation. Conclusion CSC causes oxidative damage to mitochondria.

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