Service of Physiology and Functional Explorations, Farhat HACHED Hospital, Sousse, Tunisia;
Service of Physiology and Functional Explorations, Farhat HACHED Hospital, Sousse, Tunisia.
Libyan J Med. 2014 Jun 12;9(1):23873. doi: 10.3402/ljm.v9.23873. eCollection 2014.
The mechanisms of smoking tobacco leading to chronic obstructive pulmonary disease (COPD) are beginning to be understood. However, conclusions about the role of blood or lung oxidative stress markers were disparate.
To investigate the oxidative stress in blood or lung associated with tobacco smoke and to evaluate its effect on pulmonary function data and its relation with physical activity.
It is a case-control study. Fifty-four male-smokers of more than five pack-years (PY) and aged 40-60 years were included (29 Non-COPD, 16 COPD). Physical activity score was determined. Blood sample levels of malondialdehyde (MDA), protein-cys-SH (PSH), and Glutathione (GSH) were measured. Fractional exhaled nitric oxide (FeNO) and plethysmographic measurements were performed. Correlation coefficients (r) evaluated the association between oxidative stress markers and independent variables (plethysmographic data and physical activity score).
Non-COPD (48 ± 6 years) and COPD (49 ± 5 years) groups had similar tobacco consumption patterns, that is, 27 ± 14 PY versus 30 ± 19 PY, respectively. Compared to the Non-COPD group, the COPD group had significantly lower levels of GSH and PSH, that is, mean ± SE were 40 ± 6 versus 25 ± 5 µg/mL and 54 ± 10 versus 26 ± 5 µg/g of hemoglobin, respectively. However, MDA level and FeNO values were similar. In the COPD group, none of the oxidative stress markers was significantly correlated with plethysmographic data or physical activity score. In the Non-COPD group, GSH was significantly correlated with physical activity score (r = 0.47) and PSH was significantly correlated with total lung capacity (TLC) (r = -0.50), residual volume (r = 0.41), and physical activity score (r = 0.62). FeNO was significantly correlated with TLC of the COPD group (r = -0.48).
Compared to the Non-COPD group, the COPD group had a marked decrease in blood antioxidant markers (GSH and PSH) but similar blood oxidant (MDA) or lung (FeNO) burden.
吸烟导致慢性阻塞性肺疾病（COPD）的机制开始被理解。然而，关于血液或肺部氧化应激标志物作用的结论却大相径庭。
研究与烟草烟雾相关的血液或肺部氧化应激，并评估其对肺功能数据的影响及其与体力活动的关系。
这是一项病例对照研究。共纳入 54 名吸烟超过 5 包年（PY）且年龄在 40-60 岁的男性吸烟者（29 名非 COPD 患者，16 名 COPD 患者）。测定体力活动评分。测定血液样本中丙二醛（MDA）、蛋白半胱氨酸-SH（PSH）和谷胱甘肽（GSH）的水平。进行呼出气一氧化氮（FeNO）和肺量计测量。相关系数（r）评估氧化应激标志物与独立变量（肺量计数据和体力活动评分）之间的相关性。
非 COPD 组（48±6 岁）和 COPD 组（49±5 岁）的吸烟模式相似，即分别为 27±14 PY 和 30±19 PY。与非 COPD 组相比，COPD 组的 GSH 和 PSH 水平显著降低，即分别为 40±6µg/mL 和 54±10µg/g 血红蛋白，而 MDA 水平和 FeNO 值相似。在 COPD 组中，没有一种氧化应激标志物与肺量计数据或体力活动评分显著相关。在非 COPD 组中，GSH 与体力活动评分显著相关（r=0.47），PSH 与总肺容量（TLC）（r=-0.50）、残气量（r=0.41）和体力活动评分（r=0.62）显著相关。FeNO 与 COPD 组的 TLC 显著相关（r=-0.48）。
与非 COPD 组相比，COPD 组血液抗氧化标志物（GSH 和 PSH）明显降低，但血液氧化剂（MDA）或肺部（FeNO）负荷相似。
