Abstract
Aim: Oxidant/antioxidant disequilibrium is an important problem in pathogenesis of COPD. This disequilibrium is effective in development and progression of COPD. The increased oxidative stress in COPD is not only associated with rise of oxidants but also associated with the decrease of antioxidant capacity.
Paraoxonase 1 (PON1) functions as one of the endogen free radical clearing system in human body. PON1 is localized in clara cells, endotel cells and type 1 pneumocytes of the lungs.
In this study we aimed to study the PON1 activity in COPD patients with stable condition, had acute attack and developed respiratory failure.
Material and method: Twenty five patients with stable COPD (group1) (mean age 62,9±9,4), 25 cases with acute COPD attack (group2) (mean age 63,8±9,0), 25 patients with hypercapnic respiratory failure (group3) (mean age 65,0±12,9) and 25 healthy individuals for control group (mean age 34,8±9,8), totally 100 cases, were enrolled to the study. All cases enrolled to the study underwent routine biochemical analysis including PON1 activity and lipid profile.
Results: There was significant difference between groups with respect to PON1 levels (p<0.0001). PON1 activities of COPD patient groups (group 1=96,8±57,4U/L; group 2=51,4±32,8U/L; group 3=47,1±27,5U/L) were lower than control group (185,4±110,1U/L) (p<0.0001). Also PON1 activity of stable COPD patients was higher than the COPD cases admitted with acute attack or respiratory failure (group2 and 3) (p<0.05).
Conclusion: This findings show that PON1 activity may have a role in COPD pathogenesis and endogen antioxidants might be depleted by increased oxidative stress in COPD. This also advocates that oxidative stress may have a role in acute COPD attacks.
- © 2011 ERS