Serum total sialic acid, lipid peroxidation, and glutathione reductase levels in patients with rheumatoid arthritis

The changes in the serum sialic acid levels, total lipid peroxidation products (MDA), and glutathione reductase activity were estimated in patients with rheumatoid arthritis. Serum Sialic acid is known as a parameter of inflammation. This work was undertaken to assess the potential role of sialic acid as well as oxidative stress and antioxidant status in patients with rheumatoid arthritis. Materials and methods: The levels of these parameters in serum were studied in 52 subjects with rheumatoid arthritis (study subjects) and 52 age and sex matched healthy subjects as controls. Serum total sialic acid levels were determined using the assay method described by Warren. Serum MDA was determined as the measure of thiobarbituric acid reactive substances (TBARS) and glutathione reductase activity was measured in the serum by the method described by Goldberg DM. Results: It was observed that there was a significant increase in serum sialic acid, MDA levels, and glutathione reductase activity in patients with rheumatoid arthritis compared to controls. Conclusion: The results of our study suggest higher oxygen free radical production, evidenced by increased MDA support to the oxidative stress in rheumatoid arthritis. The increased activities of antioxidant enzymes may be a compensatory regulation in response to increased oxidative stress. The results suggest the antioxidant activity of sialic acid in response to the increased oxidative stress in rheumatoid arthritis.

Anahtar Kelimeler:

malondialdehyde (MDA), glutathione reductase, rheumatoid arthritis, Sialic acid

Serum total sialic acid, lipid peroxidation, and glutathione reductase levels in patients with rheumatoid arthritis

Keywords:

Key words: Sialic acid, malondialdehyde (MDA), glutathione reductase, rheumatoid arthritis,

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1. Deborah, PM. Epidemiology of rheumatoid arthritis: determinants of onset, persistence and outcome. Clin Rheum 2002; 111: 172-7.
2. Gabriel, SE. The epidemiology of rheumatoid arthritis. Rheum Dis Clin North Am 2001; 27: 269-281.
3. Shichikawa K, Inoue K, Hirota S, Maeda A, Ota H, Kilmura M. Changes in the incidence and prevalence of rheumatoid arthritis. Ann Rheum Dis 1999; 58: 751-756.
4. Ponnio M, Alho H, Nikkari ST, Olsson U, Ryderberg U, Sillanaukee P. Serum Sialic acid in a random sample of the general population. Clin Chem 1999; 45: 1842 – 1849.
5. Kosakai O. Clinical relevance of Sialic acids determination in serum and synovial fluid in orthopaedic disorders. Rinsho Byori 1991; 39: 197 – 207.
6. Iijima R, Takahashi H, Namme R, Ikegami S, Yamazaki M. Novel biological function of sialic acid as a hydrogen peroxide scavenger. FEBS. Letters. 2004; 561: 163 – 166.
7. Plaa GL, Witschi H.Chemicals, drugs and lipid peroxidation. Ann. Rev. Pharmacol. Toxicol 1976; 16: 125-141.
8. Mapp P I, Grootveld M C. Hypoxia, oxidative stress and rheumatoid arthritis. Br. Med. Bull 1995; 51: 419-436.
9. Sato M, Miyazaki T. Antioxidants inhibit tumor necrosis factoralpha mediated stimulation of interleukin-8, monocyte chemo attractant protein-1 and collagenase expression in cultured human synovial cells. J. Rheumatol 1996; 23: 432-438.
10. Mezes M, Bartosiewicz G. Investigations on vitamin E and lipid peroxide status in rheumatic diseases. Clin. Rheumatol 1983; 2(3): 259-63.
11. Ozkan Y, Yardym-Akaydyn S, Sepici A, Keskin E, Sepici V, Simsek B. Oxidative status in rheumatoid arthritis. Clin Rheumatol 2006; 25: (Epub ahead of print).
12. Sie H. Oxidative stress: from basic research to clinical application. Am. J. Med 1991; 9: 31-38.
13. Cotgreave I, Moldeus P, Orrenius S. Host biochemical defense mechanisms against prooxidants. Annu. Rev. Pharmacol. Toxicol 1988; 28: 189-212.
14. Warren L. The thiobarbituric acid assay of Sialic acids. J Biol Chem 1959; 234: 1971 – 1975.
15. Satoh K. Serum lipid peroxide in cerebrovascular disorder determined by new colorimetric method. Clin Chim Acta 1978; 90: 37 – 43.
16. Goldberg D M., Spooner R J. Methods of enzymatic analysis. Bergmeyer H.V.3rd edn. 1983; Volume 3: p258 – 265.
17. Krishna mohan Surapaneni and v s Chandra sada gopan. Lipid peroxidation and antioxidant status in patients with rheumatoid arthritis. Indian J Clin Biochem 2008; 23 (1): 41 – 44.
18. Kajanachumpol S, Vanichapuntu M, Verasertniyom O, Totemchokchyakarn K, Vatanasuk M. Levels of plasma lipid peroxide products and antioxidant status in rheumatoid arthritis. Southeast Asian J Trop Med Public Health. 2000; 31: 335-8.
19. Tanaka K., Tokumaru S, Kojo S. Possible involvement of radical reactions in desialylation of LDL. Febs Lett 1997; 413: 202 – 224.
20. Cimen MY, Cimen OB, Kacmaz M, Ozturk HS, Yorgancioglu R, Durak I. Oxidant/antioxidant status of the erythrocytes from patients with rheumatoid arthritis. Clin Rheumatol. 2000; 19: 275-7.
21. Chandra R, Aneja R, Rewal C, Konduri R, Dass K, Agarwal S. An opium alkaloid-papaverine ameliorates ethanol induced hepatotoxicity: diminution of oxidative stress. Ind. J. Clin. Biochem. 2000 ; 15: 155-60.