Carbonic anhydrase II autoantibody and oxidative stress in rheumatoid arthritis

被引:39
作者
Alver, Ahmet [1 ]
Senturk, Ayse [1 ]
Cakirbay, Hasim [2 ]
Mentese, Ahmet [1 ]
Gokmen, Ferhat [2 ]
Keha, E. Edip [1 ]
Ucar, Fahri [3 ]
机构
[1] Karadeniz Tech Univ, Fac Med, Dept Med Biochem, TR-61080 Trabzon, Turkey
[2] Karadeniz Tech Univ, Fac Med, Dept Phys Med & Rehabil, TR-61080 Trabzon, Turkey
[3] Karadeniz Tech Univ, Fac Med, Dept Med Biol & Genet, TR-61080 Trabzon, Turkey
关键词
Carbonic anhydrase; Oxidative stress; SOD; Autoimmunity; Rheumatoid arthritis; TNF-alpha; IL-1; beta; LIPID-PEROXIDATION; ANTIBODIES; SERUM; ERYTHROCYTES; PLASMA;
D O I
10.1016/j.clinbiochem.2011.09.014
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Objectives: To investigate the relationship between carbonic anhydrase (CA) II autoantibody and lipid peroxidation, certain antioxidant parameters, and cytokines in rheumatoid arthritis (RA) patients. Design and methods: Serum levels of CA II autoantibody, cytokines (TNF alpha, IL-6, IFN-gamma, IL-beta) and bone markers (crosslaps, osteocalcine) and erythrocyte levels of antioxidant enzyme activities (SOD, CAT, GPx), GSH and MDA, and CA activities were measured in RA patients and healthy controls. Results: The CA II autoantibody titers were significantly higher (P<0.05), and erythrocyte SOD activities were significantly lower (P<0.05) in RA patients. A significant negative correlation between CA II autoantibody titers and SOD activities in RA group was established (r = -0.430, p = 0.006). The elevated cytokine levels could not be correlated with CA II autoantibody levels in RA. Conclusion: These results suggest that increased erythrocyte oxidative stress observed in RA may be effective in the mechanism of CA II autoantibody formation. (C) 2011 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.
引用
收藏
页码:1385 / 1389
页数:5
相关论文
共 33 条
  • [1] Increased serum anti-carbonic anhydrase II antibodies in patients with Graves' disease
    Alver, A.
    Mentese, A.
    Karahan, S. C.
    Erem, C.
    Keha, E. E.
    Arikan, M. K.
    Eminagaoglu, M. S.
    Deger, O.
    [J]. EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES, 2007, 115 (05) : 287 - 291
  • [2] Andoh A, 2002, INT J MOL MED, V9, P499
  • [3] [Anonymous], 1974, Catalase. Methods Enzym. Anal., DOI DOI 10.1016/B978-0-12-091302-2.50032-3
  • [4] THE AMERICAN-RHEUMATISM-ASSOCIATION 1987 REVISED CRITERIA FOR THE CLASSIFICATION OF RHEUMATOID-ARTHRITIS
    ARNETT, FC
    EDWORTHY, SM
    BLOCH, DA
    MCSHANE, DJ
    FRIES, JF
    COOPER, NS
    HEALEY, LA
    KAPLAN, SR
    LIANG, MH
    LUTHRA, HS
    MEDSGER, TA
    MITCHELL, DM
    NEUSTADT, DH
    PINALS, RS
    SCHALLER, JG
    SHARP, JT
    WILDER, RL
    HUNDER, GG
    [J]. ARTHRITIS AND RHEUMATISM, 1988, 31 (03): : 315 - 324
  • [5] Phagocytes and oxidative stress
    Babior, BM
    [J]. AMERICAN JOURNAL OF MEDICINE, 2000, 109 (01) : 33 - 44
  • [6] Effect of anti-carbonic anhydrase antibodies on carbonic anhydrases I and II
    Botrè, F
    Botrè, C
    Podestà, E
    Podda, M
    Invernizzi, P
    [J]. CLINICAL CHEMISTRY, 2003, 49 (07) : 1221 - 1223
  • [7] Evidence that cytokines play a role in rheumatoid arthritis
    Brennan, Fionula M.
    McInnes, Iain B.
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 2008, 118 (11) : 3537 - 3545
  • [8] Oxidant/antioxidant status of the erythrocytes from patients with rheumatoid arthritis
    Çimen, MYB
    Çimen, ÖB
    Kaçmaz, M
    Öztürk, HS
    Yorgancioglu, R
    Durak, I
    [J]. CLINICAL RHEUMATOLOGY, 2000, 19 (04) : 275 - 277
  • [9] Role of cytokines in rheumatoid arthritis
    Feldmann, M
    Brennan, FM
    Maini, RN
    [J]. ANNUAL REVIEW OF IMMUNOLOGY, 1996, 14 : 397 - 440
  • [10] Redox signalling and the inflammatory response in rheumatoid arthritis
    Filippin, L. I.
    Vercelino, R.
    Marroni, N. P.
    Xavier, R. M.
    [J]. CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 2008, 152 (03) : 415 - 422