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Feasibility of 8‐ OHdG formation and hOGG1 induction in PBMCs for assessing oxidative DNA damage in the lung of COPD patients
Author(s) -
Yang Shifang,
Wu Hongxu,
Zhao Junling,
Wu Xiaojie,
Zhao Jianping,
Ning Qin,
Xu Yongjian,
Xie Jungang
Publication year - 2014
Publication title -
respirology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 85
eISSN - 1440-1843
pISSN - 1323-7799
DOI - 10.1111/resp.12378
Subject(s) - copd , oxidative stress , peripheral blood mononuclear cell , medicine , biomarker , dna damage , lung , immunology , dna glycosylase , pathology , dna , in vitro , biochemistry , biology
Background and objective Oxidative stress has long been recognized to play a role in chronic obstructive pulmonary disease ( COPD ); however, approaches for assessing oxidative stress are lacking. The objective of this study was to address the feasibility of measuring 8‐oxo‐7, 8‐dihydro‐2′‐deoxyguanosine (8‐ OHdG ) formation and human 8‐oxoguanine DNA glycosylase ( hOGG1 ) induction in peripheral blood mononuclear cell ( PBMC ) to assess oxidative deoxyribonucleic acid ( DNA ) damage in the lung of smoking COPD patients. Methods PBMC were obtained from 412 participants including 129 smokers with COPD , 143 healthy smokers and 140 healthy non‐smokers. Lung tissue specimens and PBMC were obtained from smoker COPD ( n = 12), healthy smokers ( n = 12) and healthy non‐smokers ( n = 10). 8‐ OHdG and hOGG1 were detected, and correlation analysis was conducted for assessing the feasibility. Results Oxidative DNA damage (8‐ OHdG formation) along with impaired induction of hOGG1 expression in the lung was a prominent feature for smokers COPD patients. PBMC originated from smokers COPD patients also displayed similar features to that of lung tissues. Correlation analysis suggests that PBMC could be used as a surrogate for oxidative DNA damage in lung of smokers COPD patients. Indeed, 8‐ OHdG levels in PBMC DNA were negatively correlated with lung function, while hOGG1 induction in PBMC was associated with improved lung function in smokers COPD patients. Conclusions COPD patients manifest oxidative DNA damage of 8‐ OHdG along with impaired hOGG1 expression in the lung, whereas 8‐ OHdG formation and hOGG1 induction in PBMC could be a biomarker of oxidative DNA damage in the lung.