Banu ÇAVDAROĞLU, Nurgül KÖSE, Gülden BAŞKOL, Hüseyin DEMİR

Postmenopozal osteoporozlu hastalarda proteinler ve lipidlerdeki oksidatif stresin değerlendirilmesi

Objective: Oxidative stress may change cellular function in multiple pathological conditions, including osteoporosis. We aimed to determine malondialdehyde (MDA) levels, advanced oxidation protein pruducts (AOPP), levels end products of protein oxidation, thiol as known antioxidant, serum paraoxonase 1 (PON1) activities as known lipid antioxidant, induced by reactive oxygen species (ROS) for evaluating oxidative stress in osteoporotic patients. Methods: 59 patients diagnosed with postmenopaual osteoporosis were included in the study and compared with 21 healthy controls. Serum AOPP, MDA, thiol levels and PON1 activity were measured according to an enzymatic spectrophotometric method. Results: The serum MDA, AOPP, and thiol levels was significantly higher in the patient group than controls (p

Evaluation of protein and lipid oxidative stress in the patients with postmenopausal osteoporosis

Amaç: Oksidatif stres, osteoporozu da içeren pek çok patolojik durumda hücresel fonksiyonları değiştirebilir. Biz bu çalışmada postmenopozal osteoporozlu hastalarda oksidatif stresi değerlendirmek için, reaktif oksijen türleri (ROS) ile indüklenen lipid peroksidasyonu son ürünü malondialdehit (MDA), protein oksidasyonu son ürünü ileri düzey protein oksidasyonu ürünleri (AOPP), antioksidan olarak bilinen Thiol, lipid antioksidanı olarak bilinen serum paraoksonaz 1 (PON 1) aktivitesini belirlemeyi amaçladık. Yöntemler: Bu çalışmaya postmenopozal osteoporoz tanısı konan 59 hasta alındı. 21 sağlıklı kontrol grubuyla karşılaştırması yapıldı. Serum AOPP, MDA, thiol düzeyleri ve PON 1 aktivitesi enzimatik spektrofotometrik metotla ölçüldü. Bulgular: Serum MDA, AOPP ve thiol seviyeleri kontrol grubuna göre hastalarda istatistiksel olarak anlamlı derecede yüksekti (p<0,05). PON 1 aktivitesi kontrol grubuna göre hasta grubunda düşük bulundu. Sonuç: Osteoporozlu hastalarda artmış ROS düzeyleri prooksidan bir durum oluşturarak, AOPP, MDA düzeylerinin yükselmesine neden olur. Sonuç olarak lipid peroksidasyonu ve protein oksidasyonu osteoporoz patogenezinde rol oynayabilir.

PDF

___

1. Kanis JA. Osteoporosis and its consequences. in: Kanis JA (ed). Osteoporosis. BlackwelJ Science Ltd. London 1997:21.

2. Merly SL. Metabolic bone diseases. in: Kelley WH, Harris ED, Ruddy S, Sledge CB (eds), Textbook of Rheumatology. WB Saunders Company, Philadelphia 1997:563-1581.

3. Ersler WB, Harman SM, Keller ET. Immunologic aspects of osteoporosis. Dev Comp Immunol 1997;21:487-499.

4. Basu S, Michaelsson K, Olofsson H, et al. Association between oxidative stress and bone mineral density. Biochem Biophys Res Commun 2001;288:275-279.

5. Sontakke AN, Tare RS. A duality in the roles of reactive oxygen species with respect to bone metabolism. Clin Chim Acta 2002;318:145-148.

6. Varanasi SS, Francis RM, Berger CEM, et al. Mitochondrial DNA deletion associated oxidative stress and severe male osteoporosis. Osteoporos Int 1999;10:143-149.

7. Rifici V.A. Khachadırian A.K. The inhibition of low density lipoprotein oxidation by estradiol,MetaboIism 1992;41:1110-1114.

8. Cheeseman K.H., Slater, T.F. An Introduction to Free Radical Biochemistry, Brit. Med. Bulletin, 1993;149:481-93

9. De Zwart LL., Meerman JH, Commandeur JN, Vermeulen NP. Biomarkers of free radical damage aplications in experimental animals and in humans. Free Radical Biology & Medicine, 1999;26:202-226

10. Kalousova M., Skrha JT. Zima. Advanced glycoxidation end products and advanced oxidation protein products in patient with diabetes mellitus. Physiol Res. 2002; 51: 597- 604

11. Fang YZ, Yang S, Wu G. Free Radicals, Antioxidants, and Nutrition. Nutrition 2002;18:872-879.

12. Arasıl T. Günümüzde osteoporoz. In: Gökçe-Kutsal Y ed. Osteoporoz cep kitabı. Ankara, Güneş Kitabevi, 2005:1-8

13. Geusens P. Osteoporosis: Clinical Features. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH, editors. Rheumatology. Toronto: Mosby; 2003:2081-2092.

14. Biberoğlu S. Osteoporozda medikal tedavi. Prospect 1998:175-182.

15. Riggs BL, Khosla S, Melton LJ. 3rd. Sex steroids and the construction and conservation of the adult skeleton. Endocr Rev 2012;23:279302.

16. Sawada H, Ibi M, Kihara T, et al. Mechanisms of antiapoptotic effects of estrogens in nigral dopaminergic neurons. FASEB J. 2000;14:12021214.

17. Sudoh N, Toba K, Akishita M, et al.. Estrogen prevents oxidative stress-induced endothelial cell apoptosis in rats. Circulation.2001; 103:724729.

18. Dröge W. Free radicals in the physiological control of cell function. Physiol. Rev. 2002;82:4795.

19. Haddad JJ. Antioxidant and prooxidant mechanisms in the regulation of redox(y)-sensitive transcription factors. Cell Signal. 2002;14:879897.

20. Finkel T, Holbrook, N J. Nature. 2000;408:239247.

21. Sies H. Oxidative stress: introductory remarks. In: Sies H (ed); Oxidative stress. Academic Press, London 1985:1-8.

22. Polidori MC, Stahl W, Eichler O, et al. Profiles of antioxidants in human plasma. Free Radic Biol Med 2001; 30: 456.462.

23. Lean JM, Davies JT, Fuller K, et al. A crucial role for thiol antioxidants in estrogen-deficiency bone loss. J Clin Invest 2003;112:915-923.

24. Bai XC, Lu D, Liu AL, et al. Reactive oxygen species stimulates receptor activator of NF-kB ligand expression in osteoblasts. J Biol Chem 2005;280:17497-17506.

25. Bai XC, Lu D, Bai J, et al. Oxidative stress inhibits osteoblastic differentiation of bone cells by ERK and NF-kB. Biochem Biophys Res Commun 2004;314:197-207.

26. Baskol G, Demir H, Cavdaroglu B, et al. Assessment of paraoxonase 1 activity and malondialdehyde levels in patients with osteoporosis. Erc Med J 2007;29:268-273.

27. Ozgonul M, Oge A, Sezer ED, et al. The effects of estrogen and raloxifene treatment on antioxidant enzymes in brain and liver of ovarectomized female rats. Endocr Res 2003;29:183-189.

28. Aviram M, Rosenblat M, Bisgaier CL, et al. Paraoxonase inhibits high-density lipoprotein oxidation and preserves its function:a possible peroxidative role for paraoxonase. J Clin Invest 1998;101:1581-1590.

29. Parhami F. Possible role of oxidized lipids in osteoporosis: Could hyperlipidemia be a risk factor? Prostaglandins Leukot Essent Fatty Acids 2003;68:373-378.

30. Kumon Y, Nakauchi Y, Suehiro T, et al. Proinflammatory cytokines but not acute phase serum amyloid A or C- reactive protein, down regulate paraoxonase 1 (PON1) expression by Hep G2. Amyloid 2002;9:160-164.

31. Callister ME, Burke-Gaffney A, Quinlan GJ, et al. Extracellular thioredoxin levels are increased in patients with acute lung injury. Thorax 2006;61:521-527

32. Gromer S, Urig S, Becker K. The thioredoxin system -from science to clinic. Med Res Rev 2004;24:4089.

33. Burke-Gaffney A, Callister ME, Nakamura H. Thioredoxin: friend or foe in human disease? Trends Pharmacol Sci 2005;26:398404.

34. Quinlan GJ, Mumby S, Lamb NJ, et al. Acute respiratory distress syndrome secondary to cardiopulmonary bypass: Do compromised plasma iron-binding antioxidant protection and thiol levels influence outcome? Critic Care Med 2000;28:2271-2276.

35. Ohkava H, Ohishi N, Yagi K. Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction. Anal Biochem 1978;95:351-358.

36. Witko-Sarsat V, Nguyen-Khoa T, Jungers P, et al. Advanced oxidation protein products as a novel molecular basis of oxidative stress in uremia. Nephrol Dial Transplant 1999;14:76-78.

37. Eckerson HW, Romson J, Wyte C, La Du BN. The human serum paraoxonase polymorphism: identification of phenotypes by their response to salts. Am J Hum Genet 1983;35:214-227.

38. Sinaki M. Osteoporosis. In: Braddom RL ed. Pysical Medicine and Rehabilitation. Philadelphia, W.B Saunders Company, 2000:894-912.