Clinical Importance of Serum Prolidase and Carbonic Anhydrase III Levels In Patients with Stable Chronic Obstructive Pulmonary Disease

Öz

Aim: Chronic obstructive pulmonary disease (COPD) is a disease characterized by irreversible airway flow limitation and chronic airway inflammation. We aimed to investigate the clinical importance of serum prolidase enzyme, which is an indicator of collagen degradation, and Carbonic anhydrase (CA) III enzyme, which has an important function in acid-base regulation, in patients with COPD Methods : In this study, 56 stable COPD patients and 32 healthy subjects without smoking history and comorbidities were included. Serum CA III and prolidase enzyme levels were compared between the two groups. Results: The statistical difference was not found between the two groups in terms of prolidase enzyme levels (p=0.831). There was a statistically significant increase in CA III levels in the COPD group (p=0.001). There were moderate positively correlation between CAIII with partial pressure of carbon dioxide in blood (pCO2) and negatively correlation between CA III with partial pressure of oxygen in blood (pO2) in COPD patients (r:0.302, p<0.025; r:-0.314, p:0.02). Conclusions: We think that there is an important clinical relationship between CA III and COPD, and therefore, CA III may be a candidate biomarker in the follow-up of COPD.

Anahtar Kelimeler

• COPD
• prolidase
• carbonic anhydrase III
• arterial blood gase

Stabil Kronik Obtrüktif Akciğer Hastalığı Hastalarında Serum Prolidaz ve Karbonik Anhidraz III Düzeylerinin Klinik Önemi

Öz

GİRİŞ: Kronik obstrüktif akciğer hastalığı (KOAH), geri dönüşümsüz hava yolu akış kısıtlaması ve kronik hava yolu iltihabı ile karakterize bir hastalıktır. Kollajen yıkımının bir göstergesi olan serum prolidaz enzimi ile asit-baz regülasyonunda önemli işlevi olan karbonik anhidraz (CA) III enziminin KOAH'lı hastalarda klinik önemini araştırmayı amaçladık. GEREÇ VE YÖNTEM: Bu çalışmaya 56 stabil KOAH'lı hasta ile sigara öyküsü ve ek hastalığı olmayan 32 sağlıklı olgu dahil edildi. Her iki grup arasında serum CA III ve prolidaz enzim düzeyleri karşılaştırıldı. BULGULAR: Prolidaz enzim düzeyleri açısından iki grup arasında istatistiksel fark bulunmadı (p=0.831). KOAH grubunda CA III düzeylerinde istatistiksel olarak anlamlı bir artış vardı (p=0.001). KOAH hastalarında CA III enzimi düzeyi ile kanda kısmi karbondioksit basıcı (pCO2) arasında orta derecede pozitif, kanda kısmi oksijen basıncı (pO2) arasında ise negatif korelasyon vardı (r:0.302, p<0.025; r:-0.314, p:0.02). SONUÇLAR: CA III ile KOAH arasında önemli bir klinik ilişki olduğunu ve bu nedenle CA III'ün KOAH takibinde aday bir biyobelirteç olabileceğini düşünüyoruz.

Anahtar Kelimeler

• KOAH
• serum prolidaz
• karbonik anhidraz III
• arter kan gazı

Kaynakça

1. 1. Namiduru ES. Prolidase. Bratisl Lek Listy. 2016;117(8):480-5. doi: 10.4149/bll_2016_093.
2. 2. Zanaboni G, Dyne KM, Rossi A, Monafo V, Cetta G. Prolidase deficiency: biochemical study of erythrocyte and skin fibroblast prolidase activity in Italian patients. Haematologica. 1994;79(1):13-8.
3. 3. Duygu F, Koruk ST, Karsen H, Aksoy N, Taskin A, Hamidanoglu M. Prolidase and oxidative stress in chronic hepatitis C. J Clin Lab Anal. 2012;26(4):232-7. doi: 10.1002/jcla.21510.
4. 4. Şen V, Uluca Ü, Ece A, et al. Serum prolidase activity and oxidant-antioxidant status in children with chronic hepatitis B virus infection. Ital J Pediatr. 2014;40:95. doi: 10.1186/s13052-014-0095-1.
5. 5. Sayın R, Aslan M, Kucukoglu ME, et al. Serum prolidase enzyme activity and oxidative stress levels in patients with diabetic neuropathy. Endocrine. 2014;47(1):146-51. doi: 10.1007/s12020-013-0136-3.
6. 6. Pastorekova S, Parkkila S, Pastorek J, Supuran CT. Carbonic anhydrases: current state of the art, therapeutic applications and future prospects. J Enzyme Inhib Med Chem 2004;19(3):199-29. doi: 10.1080/14756360410001689540.
7. 7. Kim G, Lee TH, Wetzel P, et al. Carbonic anhydrase III is not required in the mouse for normal growth, development, and life span. Mol Cell Biol. 2004;24(22):9942-7. doi: 10.1128/MCB.24.22.9942-9947.2004. 8. Maren TH. Carbonic anhydrase: chemistry, physiology, and inhibition. Physiol Rev. 1967;47(4):595-781. doi: 10.1152/physrev.1967.47.4.595.
8. 9. Tashian RE. The carbonic anhydrases: widening perspectives on their evolution, expression and function. Bioassays 1989;10(6):186-92. doi: 10.1002/bies.950100603.

9. 10. Vaananen HK, Syrjala H, Rahkila P, et al. Serum carbonic anhydrase III and myoglobin concentrations in acute myocardial infarction. Clin Chem. 1990 4;36(4):635–8.
10. 11. Vuori J, Syrjala H, Vaananen HK. Myoglobin/carbonic anhydrase III ratio: highly specific and sensitive early indicator for myocardial damage in acute myocardial infarction. Clin Chem. 1996 1;42(1):107–9.
11. 12. Kharbanda KK, Vigneswara V, McVicker BL, et al. Proteomics reveal a concerted upregulation of methionine metabolic pathway enzymes, and downregulation of carbonic anhydrase-III, in betaine supplemented ethanol-fed rats. Biochem Biophys Res Commun. 2009 4 17;381(4):523–7. doi: 10.1016/j.bbrc.2009.02.082.
12. 13. Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global Strategy for the Diagnosis, Management and Prevention of Chronic Obstructive Pulmonary Disease: 2020 Report. [updated 2020; cited 14 april 2020]. www.goldcopd.org
13. 14. Gulbay BE, Acıcan T. Pathogenesis ve inflammation. In: Saryal S, Acıcan T. ed. Chronic Obstructive Pulmonary Disease in the light of current information. Turkey: Ankara Scientific Medicine Publishing House. 2003;p 21-33.
14. 15. Su B, Liu T, Fan H, et al. Inflammatory Markers and the Risk of Chronic Obstructive Pulmonary Disease: A Systematic Review and Meta-Analysis. PLoS One. 2016;11(4):e0150586. doi: 10.1371/journal.pone.0150586.
15. 16. Stockley RA. Neutrophils and protease/antiprotease imbalance. Am J Respir Crit Care Med. 1999;160(5 Pt 2):S49-52. doi: 10.1164/ajrccm.160.supplement_1.13.
16. 17. Tascanov MB. The Relationship Between Prolidase Activity and Atrial Electromechanical Changes in Patients with Paroxysmal Atrial Fibrillation. Comb Chem High Throughput Screen. 2019;22(1):69-75. doi: 10.2174/1386207322666190306143317.
17. 18. Bhatnager R, Nanda S, Dang AS. Plasma prolidase levels as a biomarker for polycystic ovary syndrome. Biomark Med. 2018;12(6):597-606. doi: 10.2217/bmm-2017-0306.
18. 19. Celik A, Birer MN, Kilinc M. Serum prolidase activity in systemic sclerosis. Clin Rheumatol. 2017;36(8):1827-32. doi: 10.1007/s10067-017-3677-7.
19. 20. Sertogullarindan B, Sezen H, Gunbatar H, et al. Does prolidase activity an early marker for lung emphysema in biomass smoke exposured woman. Europan respiratoy journal. 2016; 48:PA4295. DOI: 10.1183/13993003.congress-2016.PA4295
20. 21. Cakmak A, Zeyrek D, Atas A, Celik H, Aksoy N, Erel O. Serum prolidase activity and oxidative status in patients with bronchial asthma. J Clin Lab Anal. 2009;23(2):132–8. doi: 10.1002/jcla.20303.
21. 22. Gencer M, Aksoy N, Dagli EC, et al. Prolidase activity dysregulation and its correlation with oxidative-antioxidative status in chronic obstructive pulmonary disease. J Clin Lab Anal. 2011;25(1):8-13. doi: 10.1002/jcla.20347.
22. 23. Ekin S, Arısoy A, Gunbatar H, et al. The relationships among the levels of oxidative and antioxidative parameters, FEV1 and prolidase activity in COPD. Redox Rep. 2017;22(2):74-7. doi: 10.1080/13510002.2016.1139293.
23. 24. Elbehairy AF, Ciavaglia CE, Webb KA, et al; Canadian Respiratory Research Network. Pulmonary Gas Exchange Abnormalities in Mild Chronic Obstructive Pulmonary Disease. Implications for Dyspnea and Exercise Intolerance. Am J Respir Crit Care Med. 2015;191(12):1384-94. doi: 10.1164/rccm.201501-0157OC.
24. 25. Mondrup M, Anker N. Carbonic anhydrase isoenzyme B in erythrocytes of subjects with chronic acidosis. Clin Chim Acta. 1979;92(3):361-6. doi: 10.1016/0009-8981(79)90214-6.