RESUMEN
Aims: Oxidative stress is one of the major patho-physiologic hallmarks in the development of COPD. Ceruloplasmin, the major serum inhibitor of lipid peroxidation has been documented as a main extracellular antioxidant in serum and plays a role in preventing lung injury, and an abnormality in its oxidative inhibition could be involved in pathogenesis of COPD. This study aims to estimate levels of ceruloplasmin and its ferroxidase activity in COPD and compare with that in controls to explore their utility in COPD. Study Design: Comparison study. Place and Duration of Study: Department of Biochemistry, AFMC, Pune. Subjects for COPD were selected from the patients reporting with symptoms of COPD to respiratory OPD of Cardio Thoracic Centre, Pune, during Dec 2010 to Aug 2012. Methodology: Study comprised of two groups: Group I of 77 normal as controls (61 men, 16 women; age range 27-90 years) and Group II of 92 COPD patients (70 men, 22 women; age range 45 - 97 years). Both the groups were further divided into smoker and nonsmoker groups. Ferroxidase activity of ceruloplasmin was estimated by indigenous patented kinetic method of Somani and Ambade while ceruloplasmin was estimated by immunotubidimetric method using commercially available kit. Results: Serum ceruloplasmin and ferroxidase activity were significantly higher in COPD patients as compared to normal controls. Mean ± SD in COPD versus controls respectively are ceruloplasmin: 45.84 ± 12.7 mg/dL versus 37 ± 9.7 mg/dL; ferroxidase: 1324.9 ± 278.53 IU/L versus 980.5 ± 202.3 IU/L, P< .001. Statistically significant & good correlation (r > 0.7) was found between ceruloplasmin and ferroxidase in controls, nonsmoker controls and smoker controls (r = 0.76, 0.71 and 0.79 respectively) while in COPD, COPD nonsmokers and COPD smokers, no correlation was found (r = 0.00, 0.29 and 0.09 respectively). Conclusion: There is alteration in the ferroxidase activity of ceruloplasmin in COPD. Future studies with quantification of carbonyl residues or other groups in ceruloplasmin molecule leading to altered oxidative or ferroxidase activity of ceruloplasmin may provide further evidence to support a role of oxidative stress in COPD.