Oxidative Stress in osteoarthritis Cartilage; A Comparative Study
Alev Kural 1, Cemal Kural 2, Mahmut Ercan Çetinus 3, Ersin Erçin 2, Hatice Seval 4, Macit Koldaş 4
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1 Bakırkoy Dr. Sadi Konuk Eğitim Araştırma Hastanesi, Biyokimya Laboratuarı, İstanbul
2 Bakırkoy Dr. Sadi Konuk Eğitim Araştırma Hastanesi, Ortopedi ve Travmatoloji Kliniği, İstanbul
3 Haseki Eğitim Araştırma Hastanesi, Ortopedi ve Travmatoloji Kliniği, İstanbul
4 Haseki Eğitim Araştırma Hastanesi, Biyokimya Laboratuarı, İstanbul
EUR J BASIC MED SCI, Volume 4, Issue 4, pp. 83-88.
https://doi.org/10.15197/sabad.2.4.15
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ABSTRACT
The role of increased reactive oxygen species (ROS) and/or decrease in antioxidant enzyme levels in pathogenesis of osteoarthritis (OA) is controversial. In our study we investigated antioxidant enzyme activities and oxidative stress in cartilage samples of OA patients. In our study, cartilage samples were obtained from 26 subjects (18 women, 8 man) with severe hip osteoarthritis who underwent total hip replacement and as control group; cartilage samples were obtained from 25 subjects (16 women, 9 man) who underwent hemiarthroplasty for femoral neck fracture. Superoxide dismutase (SOD), glutathione peroxidase (GP), catalase (CAT) enzyme activities and lipid hydroperoxide (LPO) levels were studied with Cayman Chemical brand kits (Ann Arbor, USA). Cartilage samples of patients with hip OA had significant higher amounts of SOD, CAT and GP antioxidant enzyme activities and oxidant LPO levels (p=0.044, p=0.028, p=0.015, p=0.001 respectively). Correlation analysis showed a weak positive relationship between SOD and LPO and between CAT and LPO (r=0.426, p= 0.01; r= 0.358 p=0.002 respectively). Oxidative stress cannot be held responsible for cartilage damage in the pathogenesis of osteoarthritis as a single factor. Studies through synovial fluid analysis with more patient numbers should be helpful to understand the pathogenesis of osteoarthritis in future research.
CITATION
Kural A, Kural C, Çetinus ME, Erçin E, Seval H, Koldaş M. Oxidative Stress in osteoarthritis Cartilage; A Comparative Study. Eur J Basic Med Sci. 2014;4(4):83-8.
https://doi.org/10.15197/sabad.2.4.15
REFERENCES
- Kalpakcıoglu B, Şenel K. The interrelation of glutathione reductase, catalase, glutathione peroxidase, superoxide dismutase, and glucose-6-phosphate in the pathogenesis of rheumatoid arthritis. Clin Rheumatol 2008;27:141–5.
- Karıncaoglu Y, Batcıoglu K, Erdem T, Esrefoglu M, Genc M. The levels of plasma and salivary antioxidants in the patient with recurrent aphthous stomatitis. J Oral Pathol Med 2005;34:7–12.
- Poole A, Flint M, Brent W. Beaumont.Chondrons Extracted From Canine Tibial Cartilage : Preliminary Report on their Isolation and Structure. Journal of Orthopedic Research 1988;6:408-19.
- Poole A, Ayad S, Schofıeld R. Chondrons from articular cartilage. J Cell Sci 1988;90:635-43.
- Islamov BI, Balabanova RM, Funtikov VA. Effect of bioresonance therapy on antioxidant system in lymphocytes in patients with rheumatoid arthritis. Bull Exp Biol Med 2002;134:248–50.
- Gul M, Kutay FZ, Temocin S, Hanninen O. Cellular and clinical implications of glutathione. Indian J Exp Biol 2000;38:625–34.
- Braven J, Ansari N, Figgitt DP et al. A comparison of glutathione reductase and glutathione peroxidase activities in patients with rheumatoid arthritis and healthy adults. Br J Rheumatol 1989;8:212–5.
- Brooks PM. Impact of osteoarthritis on individuals and society: How much disability? Social consequences and health economic implications. Curr Opin Rheumatol 2002;14:573-7.
- Sutipornpalangkul W, Morales NP, Harnroongroj T. Free Radicals in Primary Knee Osteoarthritis. J Med Assoc Thai 2009;92(6):268-74.
- Aigner T, Zien A, Gehrsitz A, Gebhard PM, McKenna L. Anabolic and catabolic gene expression pattern analysis in normal versus osteoarthritic cartilage using complementary DNA-array technology. Arthritis Rheum 2001;44:2777-89.
- Hollander AP, Pidoux I, Reiner A, Rorabeck C, Bourne R, Poole AR. Damage to type II collagen in aging and osteoarthritis starts at the articular surface, originates around chondrocytes, and extends into the cartilage with progressive degeneration. J Clin Invest 1995;96:2859–69.
- Fitowska A, Ostałowska A, Dobrakowski M, et al. Protein metabolism in the synovial membrane in the hip osteoarthritis. Pol Orthop Traumatol 2012;11:77:21-6.
- Regan E, Flannelly J, Bowler R, et al. Extracellular Superoxide Dismutase and Oxidant Damage in Osteoarthritis. Arthritis Rheum 2005;52 (11):3479–91.
- Regan EA, Bowler RP, Crapo JD. Joint fluid antioxidants are decreased in osteoarthritic joints compared to joints with macroscopically intact cartilage and subacute injury. Osteoarthritis and Cartilage 2008;16:515-21.
- Fukai T, Folz RJ, Landmesser U, Harrison DG. Extracellular superoxide dismutase and cardiovascular disease. Cardiovasc Res 2002;55:239–49.
- Hapeta B, Koczy B, Fitowska A, et al. Metabolism and protein transformations in synovial membrane of a knee joint in the course of rheumatoid arthritis and degenerative arthritis. Pol Orthop Traumatol 2012;77:1-6.
- Monboisse JC, Borel JP. Oxidative damage to collagen. EXS 1992;62:323–7.
- Afonso V, Champy R, Mitrovic D, Collin P, Lomri A. Reactive oxygen species and superoxide dismutases:Role in joint diseases. Joint Bone Spine 2007;74:324-9.
- Yılmaz E, Yılmaz S, Karakurt L, Serin E. Osteoartritte nitrik oksit ve malondialdehid düzeyleri. Artroplasti Artroskopik Cerrahi Dergisi 2004;15(1):7-11.
- Sutipornpalangkul W, Morales PN, Harnroongroj T. Free radicals in primary knee osteoarthritis.J Med Assoc Thai 2009;92:268-71.
- Ostalowska A, Birkner E, Wiecha M, et al. Lipid peroxidation and antioxidant enzymes in synovial fluid of patients with primary and secondary osteoarthritis of the knee joint. Osteoarthritis Cartilage 2006;14:139-45.