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Updated: Jun 20, 2026

Isolation of Mouse Respiratory Epithelial Cells and Exposure to Experimental Cigarette Smoke at Air Liquid Interface
Published on: February 21, 2011
[Cigarette smoke-induced oxidative damage to human bronchial epithelial cells]
Shu-Kun Liu1, Ling Wangh, Chen Chen
1Department of Environmental Health, West China School of Public Health, Sichuan University, Chengdu 61004, China.
Objective:
To determine the oxidative damage of mainstream smoke (MS) on Human bronchial epithelial cells (HBE) and its role in lung cancer.
Methods:
MTT assay was used to test the cytotoxicity of MS on HBE. The HBE cells were treated with different concentrations of MS for 12 h. The chromatosome damage and DNA strand breaks were measured by micronucleus test and alkaline comet assay respectively. The contents of ROS in the HBE cells were determined using fluorescence method.
Results:
With the increase of MS, the viability of HBE cells decreased. The IC50 decreased with the increasing exposure time to MS, showing significant dose-effect and time-effect relationships. The MS induced DNA strand break in the HBE cells. The comet, L Tail, Tail DNA and OTM increased with the increase of MS concentrations. Cigarette smoke also induced chromosome damage. The micronucleus rate of the HBE cells exposed to more than one cigarette/L of MS was significantly greater than the controls (P<0.05). The ROS increased with the concentration of MS.
Conclusion:
MS induces ROS in HBE cells, resulting in increased cytotoxicity, chromosome damage and DNA strand breaks, which suggests that oxidative damage is an important mechanism of lung cancer caused by MS.
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