Oxidative stress and enzymatic antioxidant status of blood and synovial fluid in rheumatoid arthritis patients
More details
Hide details
Department of Biochemistry, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia in Katowice
Department of Orthopaedics, District Orthopaedic Hospital, Bytom
Department of Biophysics, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia in Katowice
Alina Beata Ostałowska   

MD, PhD, Department of Biochemistry, School of Medicine with the Division of Dentistry in Zabrze, Medical University of Silesia in Katowice, ul. Jordana 19, 41-808 Zabrze, tel. +48 32 272 23 18
Ann. Acad. Med. Siles. 2016;70:196–205
Although the exact etiology of rheumatoid arthritis (RA) remains unknown, there is increasing evidence that reactive oxygen species (ROS) and oxidant/antioxidant imbalance are an important part of the pathogenesis of joint tissue injury.

Material and methods:
The activities of: manganese superoxide dismutase (MnSOD) and copper-zinc superoxide dismutase (CuZnSOD) isoenzymes, catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione-S-transferase (GST), and malondialdehyde (MDA) levels were determined in blood and synovial fluid samples from 178 RA patients and from 27 healthy controls.

The RA patients showed increased antioxidant enzyme activities and MDA levels. Decreased synovial fluid viscosity was associated with a tendency for a changed antioxidant system with increased antioxidant enzyme activities, thereby suggesting a possible adaptation to ROS production in the blood and synovial fluid in RA patients.

Correlating antioxidant enzyme activities and MDA levels to disease activity might provide further information about oxidative stress in RA pathogenesis.

Ozkan Y., Yardỳm-Akadỳn S., Sepici A., Keskin E., Sepici V., Simsek B. Oxidative status in rheumatoid arthritis. Clin. Rheumatol. 2007; 26(1): 64–68.
Hitchon C.A., El-Gabalawy H.S. Oxidation in rheumatoid arthritis. Arthritis. Res. Ther. 2004; 6: 265–278.
Schiller J., Fuchs B., Arnold J., Arnold K. Contribution of reactive oxygen species to cartilage degradation in rheumatic diseases: molecular pathways, diagnosis and potential therapeutic strategies. Curr. Med. Chem. 2003; 10: 2123–2145.
Henrotin Y., Kurz B., Aigner T. Oxygen and reactive oxygen species in cartilage degradation: friends or foes? Osteoarthritis Cartilage 2005; 13: 643––654.
Henrotin Y.E., Bruckner P., Pujol J.P. The role of reactive oxygen species in homeostasis and degradation of cartilage. Osteoarthritis Cartilage 2003; 11: 747–755.
Kamanli A., Naziroglu M., Aydilek N., Hacievliyagil C. Plasma lipid peroxidation and antioxidant levels in patients with rheumatoid arthritis. Cell. Biochem. Funct. 2004; 22: 53–57.
Çimen M.Y.B., Çimen Ö.B., Kaçmaz M., Öztürk H.S., Yorgancioğlu R., Durak Ì. Oxidant/antioxidant status of the erythrocytes from patients with rheumatoid arthritis. Clin. Rheumatol. 2000; 19: 275–277.
Taysi S., Polat F., Gul M., Sari R.A., Bakan E. Lipid peroxidation, some extracellular antioxidants, and antioxidant enzymes in serum of patients with rheumatoid arthritis. Rheumatol. Int. 2002; 21: 200–204.
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: 324–329.
Gambhir J.K., Lali P., Jain A.K. Correlation between blood antioxidant levels and lipid peroxidation in rheumatoid arthritis. Clin. Biochem. 1997; 30: 351–355.
Aletaha D., Ward M.M., Machold K.P., Nell V.P., Stamm T., Smolen J.S. Remission and active disease in rheumatoid arthritis: Defining criteria for disease activity states. Arthritis Rheum 2005; 52(9): 2625–2636.
Terčič D., Božič B. The basis of the synovial fluid analysis. Clin. Chem. Lab. Med . 2001; 39: 1221–1226.
Ostałowska A., Birkner E., Wiecha M., Kasperczyk S., Kasperczyk A., Kapołka D., Zon-Giebel A. Lipid peroxidation and antioxidant enzymes in synovial fluid of patients with primary and secondary osteoarthritis of the knee joint. Osteoarthritis Cartilage 2006; 14: 139–145.
Yamazaki K., Fukuda K., Matsukawa M., Hara F., Matsushita T., Yamamoto N., Yoshida K., Munakata H., Humanishi C. Cyclic tensile stretch loaded on bovine chondrocytes causes depolymerization of hyaluronan: involvement of reactive oxygen species. Arthritis. Rheum. 2003; 48: 3151–3158.
Cedergren J., Forslund T., Sundqvist T., Skogh T. Intracellular oxidative activation in synovial fluid neutrophils from patients with rheumatoid arthritis but not from other arthritis patients. J. Rheumatol. 2007; 34: 2162–2170.
Robinson J., Watson F., Bucknall R.C., Edwards S.W. Activation of neutrophil reactive-oxidant production by synovial fluid from patients with inflammatory joint disease. Soluble and insoluble immunoglobulin aggregates activate different pathways in primed and unprimed cells. Biochem. J. 1992; 286: 345–351.
Borsiczky B., Szabo Z., Jaberansari M.T., Mack P.P., Röth E. Activated PMNs lead to oxidative stress on chondrocytes: a study of swine knees. Acta Orthop. Scand. 2003; 74: 190–195.
Mazzetti I., Grigolo B., Pulsatelli L., Dolzani P., Silvestri T., Roseti L., Meliconi R., Facchini A. Differential roles of nitric oxide and oxygen radicals in chondrocytes affected by osteoarthritis and rheumatoid arthritis. Clin. Sci. 2001; 101: 593–599.
Tiku M.L., Yan Y.P., Chen K.Y. Hydroxyl radical formation in chondrocytes and cartilage as detected by electron paramagnetic resonance spectroscopy using spin trapping reagents. Free Radic. Res. 1998; 29: 177–187.
Tanabe T., Otani H., Mishima K., Ogawa R., Inagaki C. Phorbol 12-myristate 13-acetate (PMA)-induced oxyradical production in rheumatoid synovial cells. Jpn. J. Pharmacol. 1997; 73: 347–351.
Carlo M.D., Loeser R.F. Increased oxidative stress with aging reduces chondrocyte survival: correlation with intracellular glutathione levels. Arthritis Rheum. 2003; 48: 3419–3430.
Borsiczky B., Zadravecz G., Röth E. Haemarthros induced articular cartilage degradation. Acta Chir. Hung. 1997; 36: 43–45.
Dabbagh A.J., Trenam C.W., Morris C.J., Blake D.R. Iron in joint inflammation. Ann. Rheum. Dis. 1993; 52: 67–73.
Takahashi T., Tominaga K., Takano H., Ariyoshi W., Habu M., Fukuda J., Maeda H. A decrease in the molecular weight of hyaluronic acid in synovial fluid from patients with temporomandibular disorders. J. Oral. Pathol. Med. 2004; 33: 224–229.
Alpaslan C., Bilgihan A., Alpaslan G.H., Güner B., Ozgür Yis M., Erbaş D. Effect of arthrocentesis and sodium hyaluronate injection on nitrite, nitrate, and thiobarbituric acid-reactive substance levels in the synovial fluid. Oral. Surg. 2000; 89: 686–690.
Bae S.C., Kim S.J., Sung M.K. Inadequate antioxidant nutrient intake and altered plasma antioxidant status of rheumatoid arthritis patients. J. Am. Coll. Nutr. 2003; 22: 311–315.
Sarban S., Kocyigit A., Yazar M., Isikan U. Plasma total antioxidant capacity, lipid peroxidation, and erythrocyte antioxidant enzyme activities in patients with rheumatoid arthritis and osteoarthritis. Clin. Biochem. 2005; 38: 981–986.
Ostałowska A., Kasperczyk S., Kasperczyk A., Słowińska L., Marzec M., Stołtny T. et al. Oxidant and anti-oxidant systems of synovial fluid from patients with knee post-traumatic arthritis. J. Orthop. Res. 2007; 25: 804–812.
Grisham M.B. Reactive oxygen species in immune responses. Free Rad. Biol. Med. 2004; 36: 1479–1480.