Lipid, protein, DNA oxidation and antioxidant status in rheumatoid arthritis

To investigate lipid, protein, DNA oxidation and antioxidant status in blood and synovial fluid of rheumatoid arthritis (RA) patients and to determine the importance of oxidative stress parameters in reflecting disease activity. 20 RA patients and 15 healthy controls were included. Lipid peroxidatio...

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Bibliographic Details
Published in:Clinical biochemistry Vol. 41; no. 7; pp. 538 - 543
Main Authors: Seven, Arzu, Güzel, Savaş, Aslan, Mahmure, Hamuryudan, Vedat
Format: Journal Article
Language:English
Published: United States Elsevier Inc 01-05-2008
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Summary:To investigate lipid, protein, DNA oxidation and antioxidant status in blood and synovial fluid of rheumatoid arthritis (RA) patients and to determine the importance of oxidative stress parameters in reflecting disease activity. 20 RA patients and 15 healthy controls were included. Lipid peroxidation (thiobarbituric acid reactive substances (TBARS), lipid hydroperoxide, and conjugated diene), protein oxidation (carbonyl and thiol), DNA oxidation (8-OHdG) and antioxidant status markers (glutathione (GSH), glutathione peroxidase (GSH Px), superoxide dismutase (CuZn SOD), and catalase) were determined in blood and synovial fluid. TBARS ( p < 0.001), lipid hydroperoxide ( p < 0.001), conjugated diene ( p < 0.001), carbonyl ( p < 0.001) and 8-OHdG ( p < 0.01) levels were significantly higher; thiol ( p < 0.01) and GSH levels ( p < 0.01) and GSH Px ( p < 0.001) and CuZn SOD ( p < 0.01) activities were significantly lower in blood of RA patients. TBARS ( p < 0.001), lipid hydroperoxide ( p < 0.001), conjugated diene ( p < 0.01), carbonyl ( p < 0.001) and 8-OHdG ( p < 0.05) levels were significantly higher, catalase activity ( p < 0.001) significantly lower in synovial fluid of RA patients. Increased lipid, protein and DNA oxidation markers and impaired antioxidant status confirm the role of oxidative stress in the pathogenesis of RA. Lipid peroxidation markers can serve as surrogate markers for disease activity.
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ISSN:0009-9120
1873-2933
DOI:10.1016/j.clinbiochem.2008.01.029