The oxidant-antioxidant imbalance is an important factor in the pathogenesis of COPD and yet there is a lack of evidence about total antioxidant levels of COPD patients, which may provide valuable information about the prognosis of the disease. In this study, we aimed to evaluate and compare the oxidant-antioxidant systems in healthy controls and in COPD patients with a stable disease and during an acute exacerbation. The study was conducted with 42 COPD patients diagnosed by a pulmonologist and 21 healthy volunteers. Pulmonary function tests were performed, arterial blood gas; white blood cell, hemoglobin, hematocrit, platelet, neutrophil%, MCV, CRP, and sedimentation rate results were compared with total antioxidant status, total oxidant status levels, and oxidative stress index. There was a statistically significant difference between the three groups in $FEV_1/FVC$ , $FEV_1$ , FVC, $pCO_2$ , $pO_2$ , $\%SpO_24 , white blood cell count, neutrophil %, CRP, and ESR values. In regard to oxidant-antioxidant system measurements there was no statistically significant difference in TAS levels, but there was a significant difference in TOS and oxidative stress index levels. Positive correlation between WBC and TOS was detected in the analysis performed and no correlation was found in other parameters. Our study showed that the measurement of TAS, TOS and OSI were meaningful parameters in the evaluation of oxidative imbalance. Oxidant stress was found to be significantly increased in all COPD patients, especially in patients with COPD exacerbations. Despite the increase in oxidative stress, no increase in antioxidant levels was observed in COPD patients.
___
1. Global Strategy for the Diagnosis, Management and Prevention of COPD, Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2019.
2. Church DF, Pryor WA. Free-radical chemistry of cigarette smoke and its toxicological implications. Environ Health Perspect. 1985;64:111-26.
3. Pryor WA, Godber SS. Noninvasive measures of oxidative stress status in humans. Free Radic Biol Med. 1991;10:177-84.
4. Repine JE, Bast A, Lankhorst I. Oxidative stress in chronic obstructive pulmonary disease. Oxidative Stress Study Group. Am J Respir Crit Care Med. 1997;156:341-57.
5. Yang W, Block ER. Effect of hypoxia and reoxygenation on the formation and release of reactive oxygen species by porcine pulmonary artery endothelial cells. J Cell Physiol. 1995;164:414-23.
6. Jacob RA, Burri BJ. Oxidative damage and defense. Am J Clin Nutr. 1996;63:985-90.
7. Raha S, Robinson BH. Mitochondria, oxygen free radicals, disease and ageing. Trends Biochem Sci. 2000;25:502-8.
8. Cochrane CG. Cellular injury by oxidants. Am J Med. 1991;91:23-30.
9. Özlü T, KOAH Patogenezi. In: Solunum sistemi ve hastalıkları Temel başvuru kitabı. Cilt 2. İstanbul: İstanbul Medikal Yayıncılık. 2010. p. 1511, 2011. p. 12.
10. 10. Saryal B, Acıcan T. KOAH Etyopatogenezi. In: Güncel Bilgiler Işığında Kronik Obstrüktif Akciğer Hastalığı. Bilimsel Tıp Yayınevi, Ankara, 2003.
11. Faul F, Erdfelder E, Buchner A, et al. Statistical power analyses using G* Power 3.1: Tests for correlation and regression analyses. Behav Res Methods. 2009;41:1149-60.
12. Rijcken B, Britton J. Epidemiology of chronic obstructive pulmonary disease. Eur Respir Mon 1998;7:41–73.
13. Erel O. A novel automated method to measure total antioxidant response against potent free radical reactions. Clin Biochem. 2004;37:112-9.
14. Erel O. A new automated colorimetric method for measuring total oxidant status. Clin Biochem. 2005;38:1103-11.
15. Domej W, Oetti K, Renner W. Oxidative stress and free radicals in COPD– implications and relevance for treatment. Int J Chron Obstruct Pulmon Dis. 2014;9:1207-24.
16. 16. Barnes PJ et al. Reactive Oxygen Species. In: Asthma and COPD: basic mechanisms and clinical management. Elsevier, 2009.
17. World Health Organization. Obesity: preventing and managing the global epidemic. World Health Organization, 2000.
18. Musaad S, Haynes EN. Biomarkers of obesity and subsequent cardiovascular events. Epidemiol Rev. 2007;29:98-114.
19. Inal ME, Kanbak G, Sunal E. Antioxidant enzyme activities and malondialdehyde levels related to aging. Clin Chim Acta. 2001;305:75-80.
20. Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease. American Thoracic Society. Am J Respir Crit Care Med. 1995;152:S77-121.
21. Koltas IS, Yucebilgic G, Bilgin R, et al. Serum Malondialdehyde level in patients with cystic echinococcosis. Saudi Med J. 2006;27:1703-5.
22. Yorulmaz Demir A, Metin A Işıkoglu S, et al. The effect of isotretinoin on oxidative stress in severe acne vulgaris patients. Turkiye Klinikleri J Med Sci. 2012;32:1026-31.
23. Tug T, Terzi SM, Sari N, et al. Evaluation of lipid peroxidation and erythrocyte catalase levels of asthmatic patients in acute attack and stable state. Eurasian J Pulmonol. 2004;6:220-5.
24. Hu G, Cassano PA. Antioxidant nutrients and pulmonary function: the Third National Health and Nutrition Examination Survey (NHANES III). Am J Epidemiol. 2000;151:975-81.
25. Schwartz J, Weiss ST. Relationship between dietary vitamin c intake and pulmonary function in the first national health and nutrition examination survey (NHANES I). Am J Clin Nutr. 1994;59:110-4.
26. Tug T, Terzi SM, Ozdemir N, et al. Evaluation of oxidative mechanisms in acute exacerbation and stable period in the patients with chronic obstructive pulmonary disease. Toraks Dergisi. 2003;4:12-15.
27. Tug T, Karatas F, Terzi SM. Antioxidant vitamins (a, c and e) and malondialdehyde levels in acute exacerbation and stable periods of patients with chronic obstructive pulmonary disease. Clin Invest Med. 2004;27:123-8.