Abstract
Paraoxonase 1 (PON1) and arylesterase (ARE) enzymes have an important role in the prevention of oxidative stress which is related to the pathogenesis of chronic obstructive pulmonary disease (COPD). PON1 levels vary widely among individuals and ethnic groups, which is in part associated with polymorphisms. We investigated PON1 and ARE activity and phenotype distribution in COPD patients and healthy individuals. Sixty six COPD patients and 59 control subjects were involved in the study. Serum PON1 and ARE activities were detected by spectrophotometric method. The ratio of salt-induced PON1 to ARE activity was used to determine phenotypes as QQ, QR, and RR. COPD patients exhibited higher PON1 activity (199.1 vs 129.2, p=0.002) but lower ARE activity compared to control (21.3 vs 33.5, p=0.021). There was a significant difference between COPD and control group with respect to PON1 phenotype characteristics. RR phenotypic distribution was more common in the COPD group than in control (60.6% [95% CI: 48.8 - 72.3] versus 22.0 % [95% CI: 12.0 - 31.9], p=0.001). We also found that smoking (95.0% CI: 0.001-0.036, p<0.001) and RR phenotype (95.0% CI: 0.006 - 0.59, p=0.016) are independent determinants in COPD. We found that RR phenotype was more common in COPD patients compared to control. Smoking and RR phenotype may be defined as independent factors associated with COPD.
Highlights
Chronic obstructive pulmonary disease (COPD) is one of the most important causes of mortality and morbidity across the globe [1]
There was a significant difference between COPD and control group with respect to Paraoxonase 1 (PON1) phenotype characteristics
RR phenotypic distribution was more common in the COPD group than in control (60.6% [95% CI: 48.8 - 72.3] versus 22.0 % [95% CI: 12.0 - 31.9], p=0.001)
Summary
Chronic obstructive pulmonary disease (COPD) is one of the most important causes of mortality and morbidity across the globe [1]. It is characterized by enhanced chronic inflammatory response in the airway to toxic particles or gases [1, 2]. Many inflammatory cells and cytokines have a role in the pathogenesis of COPD. Environmental risk factors such as smoking, air pollution, and biomass affect the genome of susceptible individuals and trigger the onset of the disease [3]. Definition of clinical phenotypes is needed to facilitate the understanding of pathogenesis and management of the disease [4]
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