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Yıl 2019, Cilt: 5 Sayı: 5, 740 - 744, 04.09.2019
https://doi.org/10.18621/eurj.414367

Öz

Kaynakça

  • [1] Felson D. The epidemiology of osteoarthritis: prevalence and risk factors. In: Kuettner KE, Goldberg VM, eds. Osteoarthritic Disorders. Rosemont, IL: American Academy of Orthopaedic Surgeons; 1995:13-24.
  • [2] Petersson IF. Occurrence of osteoarthritis of the peripheral joints in European populations. Ann Rheum Dis 1996;55:659-61.
  • [3] Ertürk C, Altay MA, Selek S, Koçyiğit A. Paraoxonase-1 activity and oxidative status in patients with knee osteoarthritis and their relationship with radiological and clinical parameters. Scand J Clin Lab Invest 2012;72:433-9.
  • [4] Brandt KD, Dieppe P, Radin EL. Commentary: Is it useful to subset “primary” osteoarthritis? A critique based on evidence regarding the etiopathogenesis of osteoarthritis. Semin Arthritis Rheum 2009;39:81-95.
  • [5] Soran N, Altindag O, Cakir H, Celik H, Demirkol A, Aksoy N. Assessment of paraoxonase activities in patients with knee osteoarthritis. Redox Rep. 2008;13:194-8.
  • [6] Altindag O, Erel O, Aksoy N, Selek S, Celik H, Karaoglanoglu M. Increased oxidative stress and its relation with collagen metabolism in knee osteoarthritis. Rheumatol Int. 2007;27:339-44.
  • [7] Ziskoven C, Jäger M, Zilkens C, Bloch W, Brixius K, Krauspe R. Oxidative stress in secondary osteoarthritis: from cartilage destruction to clinical presentation? Orthop Rev (Pavia) 2010;2:e23.
  • [8] Davies CM, Guilak F, Weinberg JB, Fermor B. Reactive nitrogen and oxygen species in interleukin-1-mediated DNA damage associated with osteoarthritis. Osteoarthritis Cartilage 2008;16:624-30.
  • [9] Martel-Pelletier J, Pelletier JP. Is osteoarthritis a disease involving only cartilage or other articular tissues? Eklem Hastalik Cerrahisi 2010;21:2-14.
  • [10] Kayalı R, Çakatay U. [Basic mechanisms of protein oxidation]. Cerrahpaşa J Med 2004;35: 83-9. [Article in Turkish]
  • [11] Ustundag Y, Huysal K, Kahvecioglu K, Demirci H, Yavuz S, Sambel M, et al. Establishing reference values and evaluation of an in-house ferric reducing antioxidant power (FRAP) colorimetric assay in microplates. Eur Res J 2016;2:126-31.
  • [12] Sen CK, Packer L. Thiol homeostasis and supplements in physical exercise. Am J Clin Nutr 2000;72(2 Suppl.):653S-69S.
  • [13] Turell L, Radi R, Alvarez B. The thiol pool in human plasma: the central contribution of albumin to redox processes. Free Radic Biol Med 2013;65:244-53.
  • [14] Jones DP, Liang Y. Measuring the poise of thiol/disulfide couples in vivo. Free Radic Biol Med 2009; 47:1329-38.
  • [15] Circu ML, Aw TY. Reactive oxygen species, cellular redox systems, and apoptosis. Free Radic Biol Med 2010;48:749-62.
  • [16] Biswas S, Chida AS, Rahman I. Redox modifications of protein-thiols: emerging roles in cell signaling. Biochem Pharmacol 2006;71:551-64.
  • [17] Ellman G, Lysko H. A precise method for the determination of whole blood and plasma sulfhydryl groups. Anal Biochem 1979;93:98-102.
  • [18] Erel O, Neselioglu S. A novel and automated assay for thiol/disulphide homeostasis. Clin Biochem 2014;47:326-32.
  • [19] Altman R, Asch E, Bloch D, Bole G, Borenstein D, Brandt K, et al. Development of criteria for the classification and reporting of osteoarthritis. Classification of osteoarthritis of the knee. Diagnostic and therapeutic criteria committee of the American Rheumatism Association. Arthritis Rheum 1986;29:1039-49.
  • [20] Kellgren JH, Lawrence JS. Radiological assessment of osteoarthrosis. Ann Rheum Dis 1957;16:494-502.
  • [21] Rodrigues SD, Batista GB, Ingberman M, Pecoits-Filho R, Nakao LS. Plasma cysteine/cystine reduction potential correlates with plasma creatinine levels in chronic kidney disease. Blood Purif 2012;34:231-7.
  • [22] Prabhu A, Sarcar B, Kahali S, Yuan Z, Johnson JJ, Adam KP, et al. Cysteine catabolism: a novel metabolic pathway contributing to glioblastoma growth. Cancer Res 2014;74:787-96.
  • [23] Eroğlu O, Dindar Badem N, Baccıoğlu A, Cömertpay E, Neşelioğlu S, Erel Ö. Significance of thiol/disulphide homeostasis and ischemia modified albumin levels in chronic obstructive pulmonary disease. Eur Res J 2019;5:250-7.
  • [24] Yudoh K, Nguyen T, Nakamura H, Hongo-Masuko K, Kato T, Nishioka K. Potential involvement of oxidative stress in cartilage senescence and development of osteoarthritis: oxidative stress induces chondrocyte telomere instability and downregulation of chondrocyte function. Arthritis Res Ther 2005;7:R380-91.
  • [25] Martin JA, Brown TD, Heiner AD, Buckwalter JA. Chondrocyte senescence, joint loading and osteoarthritis. Clin Orthop Relat Res 2004;427 Suppl:S96-103.

Dynamic thiol-disulphide homeostasis in grade 3-4 gonarthrosis

Yıl 2019, Cilt: 5 Sayı: 5, 740 - 744, 04.09.2019
https://doi.org/10.18621/eurj.414367

Öz

Objective:
We
aimed to determine thiol-disulphide homeostasis, which plays a vital role and
to investigate the relationship among homeostatic parameters and disease.

Methods: In
this prospective study, we enrolled 38 patients with osteoarthritis (31 females
and 7 males) and 38 healthy controls (30 females, 8 males volunteers).
Diagnosis of osteoarthritis was made according to the American College of
Rheumatology Criteria. The severity of osteoarthritis was assessed and
classified according to the Kellgren-Lawrence grading scale.

Results: The
mean age was 63.8 (range; 53-74) years in the osteoarthritis group and 65.6 (range;
55-75) years in the control group. There were no significant differences
between the patients and controls in respect to age, gender and body mass index
(
p > 0.05). Serum albumin (p = 0.605) and total protein levels (p = 0.605) between patients and controls
were similar. In the osteoarthritis group disulphide/ native thiol percent
ratios and disulphide/ total thiol percent ratios were found to be
statistically higher (
p = 0.002 and p = 0.002; respectively) and
native/ total thiol percent ratios were significantly lower than that of the
control group (
p = 0.002).







Conclusions: Thiol-disulphide
homeostasis is weakened in osteoarthritis, and the balance shifts to the
disulphide bond formation side. Substitution of thiol deficiency and correction
of thioldisulphide imbalance may be beneficial in the managing treatment of the
disease. Further studies may be needed for evaluating articular fluid
thiol-disulphide homeostasis. 

Kaynakça

  • [1] Felson D. The epidemiology of osteoarthritis: prevalence and risk factors. In: Kuettner KE, Goldberg VM, eds. Osteoarthritic Disorders. Rosemont, IL: American Academy of Orthopaedic Surgeons; 1995:13-24.
  • [2] Petersson IF. Occurrence of osteoarthritis of the peripheral joints in European populations. Ann Rheum Dis 1996;55:659-61.
  • [3] Ertürk C, Altay MA, Selek S, Koçyiğit A. Paraoxonase-1 activity and oxidative status in patients with knee osteoarthritis and their relationship with radiological and clinical parameters. Scand J Clin Lab Invest 2012;72:433-9.
  • [4] Brandt KD, Dieppe P, Radin EL. Commentary: Is it useful to subset “primary” osteoarthritis? A critique based on evidence regarding the etiopathogenesis of osteoarthritis. Semin Arthritis Rheum 2009;39:81-95.
  • [5] Soran N, Altindag O, Cakir H, Celik H, Demirkol A, Aksoy N. Assessment of paraoxonase activities in patients with knee osteoarthritis. Redox Rep. 2008;13:194-8.
  • [6] Altindag O, Erel O, Aksoy N, Selek S, Celik H, Karaoglanoglu M. Increased oxidative stress and its relation with collagen metabolism in knee osteoarthritis. Rheumatol Int. 2007;27:339-44.
  • [7] Ziskoven C, Jäger M, Zilkens C, Bloch W, Brixius K, Krauspe R. Oxidative stress in secondary osteoarthritis: from cartilage destruction to clinical presentation? Orthop Rev (Pavia) 2010;2:e23.
  • [8] Davies CM, Guilak F, Weinberg JB, Fermor B. Reactive nitrogen and oxygen species in interleukin-1-mediated DNA damage associated with osteoarthritis. Osteoarthritis Cartilage 2008;16:624-30.
  • [9] Martel-Pelletier J, Pelletier JP. Is osteoarthritis a disease involving only cartilage or other articular tissues? Eklem Hastalik Cerrahisi 2010;21:2-14.
  • [10] Kayalı R, Çakatay U. [Basic mechanisms of protein oxidation]. Cerrahpaşa J Med 2004;35: 83-9. [Article in Turkish]
  • [11] Ustundag Y, Huysal K, Kahvecioglu K, Demirci H, Yavuz S, Sambel M, et al. Establishing reference values and evaluation of an in-house ferric reducing antioxidant power (FRAP) colorimetric assay in microplates. Eur Res J 2016;2:126-31.
  • [12] Sen CK, Packer L. Thiol homeostasis and supplements in physical exercise. Am J Clin Nutr 2000;72(2 Suppl.):653S-69S.
  • [13] Turell L, Radi R, Alvarez B. The thiol pool in human plasma: the central contribution of albumin to redox processes. Free Radic Biol Med 2013;65:244-53.
  • [14] Jones DP, Liang Y. Measuring the poise of thiol/disulfide couples in vivo. Free Radic Biol Med 2009; 47:1329-38.
  • [15] Circu ML, Aw TY. Reactive oxygen species, cellular redox systems, and apoptosis. Free Radic Biol Med 2010;48:749-62.
  • [16] Biswas S, Chida AS, Rahman I. Redox modifications of protein-thiols: emerging roles in cell signaling. Biochem Pharmacol 2006;71:551-64.
  • [17] Ellman G, Lysko H. A precise method for the determination of whole blood and plasma sulfhydryl groups. Anal Biochem 1979;93:98-102.
  • [18] Erel O, Neselioglu S. A novel and automated assay for thiol/disulphide homeostasis. Clin Biochem 2014;47:326-32.
  • [19] Altman R, Asch E, Bloch D, Bole G, Borenstein D, Brandt K, et al. Development of criteria for the classification and reporting of osteoarthritis. Classification of osteoarthritis of the knee. Diagnostic and therapeutic criteria committee of the American Rheumatism Association. Arthritis Rheum 1986;29:1039-49.
  • [20] Kellgren JH, Lawrence JS. Radiological assessment of osteoarthrosis. Ann Rheum Dis 1957;16:494-502.
  • [21] Rodrigues SD, Batista GB, Ingberman M, Pecoits-Filho R, Nakao LS. Plasma cysteine/cystine reduction potential correlates with plasma creatinine levels in chronic kidney disease. Blood Purif 2012;34:231-7.
  • [22] Prabhu A, Sarcar B, Kahali S, Yuan Z, Johnson JJ, Adam KP, et al. Cysteine catabolism: a novel metabolic pathway contributing to glioblastoma growth. Cancer Res 2014;74:787-96.
  • [23] Eroğlu O, Dindar Badem N, Baccıoğlu A, Cömertpay E, Neşelioğlu S, Erel Ö. Significance of thiol/disulphide homeostasis and ischemia modified albumin levels in chronic obstructive pulmonary disease. Eur Res J 2019;5:250-7.
  • [24] Yudoh K, Nguyen T, Nakamura H, Hongo-Masuko K, Kato T, Nishioka K. Potential involvement of oxidative stress in cartilage senescence and development of osteoarthritis: oxidative stress induces chondrocyte telomere instability and downregulation of chondrocyte function. Arthritis Res Ther 2005;7:R380-91.
  • [25] Martin JA, Brown TD, Heiner AD, Buckwalter JA. Chondrocyte senescence, joint loading and osteoarthritis. Clin Orthop Relat Res 2004;427 Suppl:S96-103.
Toplam 25 adet kaynakça vardır.

Ayrıntılar

Birincil Dil İngilizce
Konular Biyokimya ve Hücre Biyolojisi (Diğer), Ortopedi, Romatoloji ve Artrit
Bölüm Original Article
Yazarlar

Kenan Güvenç 0000-0002-1742-3953

Şahap Cenk Altun 0000-0003-0155-1384

Merve Ergin 0000-0003-3440-3353

Özcan Erel 0000-0002-2996-3236

Faik İlik 0000-0002-4889-1653

Yayımlanma Tarihi 4 Eylül 2019
Gönderilme Tarihi 11 Nisan 2018
Kabul Tarihi 26 Eylül 2018
Yayımlandığı Sayı Yıl 2019 Cilt: 5 Sayı: 5

Kaynak Göster

AMA Güvenç K, Altun ŞC, Ergin M, Erel Ö, İlik F. Dynamic thiol-disulphide homeostasis in grade 3-4 gonarthrosis. Eur Res J. Eylül 2019;5(5):740-744. doi:10.18621/eurj.414367

e-ISSN: 2149-3189 


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