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[Smoking, the level of DNA adducts and chronic obstructive pulmonary diseases]
Jun-gang Xie1, Yong-jian Xu, Zhen-xiang Zhang
1Department of Respiratory Medicine, Tongji Hospital of Tongji Medical College, Huazhong Science and Technology University, Wuhan 430030, China.
Objective:
To investigate the association between DNA adducts (DNA-BPDE) and smoking, and the association of DNA adducts with the development of chronic obstructive pulmonary disease (COPD).
Methods:
DNA-BPDE were tested with competitive enzyme-linked immunosorbent assay (ELISA) in passive smoking rats. DNA-BPDE were also tested in 68 people including smokers and non-smokers, and in 88 patients with COPD and 87 healthy smoking control subjects. Pre- and post-stimulation with benzo[a]pyrene diol epoxide (BPDE), DNA-BPDE of lymphocytes were tested in 20 patients with COPD and 20 healthy smoking control subjects. The dynamic process of apoptosis was analyzed by flow cytometry.
Results:
(1) Smoking and DNA-BPDE: (1) With more days of passive smoking, the level of DNA-BPDE in rats increased, the correlation coefficient being 0.90. (2) With increasing of smoking index, the level of DNA-BPDE increased in the 68 healthy people, the correlation coefficient being 0.67. (2) DNA-BPDE and COPD: In patients with COPD and the controls, DNA-BPDE (per 10(7) nucleotides) were 91 +/- 23 and 67 +/- 15, the difference being significant (P < 0.01). Pre- and post-stimulation with BPDE, the DNA-BPDE were 94.5 +/- 24.1 and 106.1 +/- 27.3 in the 20 patients with COPD, but these were 68.3 +/- 15.8 and 72.5 +/- 16.7 in the controls. The difference between pre- and post-stimulation in the COPD group and the healthy smoking control group was significant (P < 0.01). (3) The apoptosis rate of T-lymphocytes and B-lymphocytes were 18.5% +/- 3.1% and 5.8% +/- 0.6% in COPD, but were 9.5% +/- 1.8% and 5.2% +/- 0.7% in the healthy smoking control subjects, the difference being significant (P < 0.01).
Conclusions:
There is a significant association between the levels of DNA-BPDE and smoking. DNA-BPDE may result in cell damage and cell apoptosis, and may contribute to the pathogenesis of COPD.
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