Home Lipid peroxidation and homocysteine levels in Behçet's disease
Article
Licensed
Unlicensed Requires Authentication

Lipid peroxidation and homocysteine levels in Behçet's disease

  • A. Görkem Mungan , Murat Can , Serefden Açikgöz , Emel Eştürk and Cevdet Altinyazar
Published/Copyright: September 8, 2006

Abstract

Background: The aim of this study was to investigate serum paraoxonase (PON1) activity in relation to homocysteine, malondialdehyde (MDA) and lipid parameters in active and inactive Behçet's disease (BD).

Methods: A total of 46 consecutive BD patients and 25 healthy control subjects were included in the present study.

Results: Serum PON1 activity in both active and inactive BD was significantly lower compared with healthy subjects (p<0.05). When compared to the control group, serum MDA levels were significantly higher in both active and inactive BD (p<0.05). Serum C-reactive protein (CRP) and homocysteine concentrations were significantly higher in active BD than those in inactive BD and control subjects (p<0.05). In addition, there was significant negative correlation between serum PON1 and MDA levels (r=−0.697, p<0.05) and serum PON1 activity was also negatively correlated with homocysteine levels (r=−0.428, p<0.05) in BD patients.

Conclusions: Decreased PON1 could explain the increased lipid peroxidation and oxidative stress observed in BD. Also, according to our results, we suggest that homocysteine may contribute to decreased serum PON1 activity.

Clin Chem Lab Med 2006;44:1115–8.


Corresponding author: Murat Can, Karaelmas University, Faculty of Medicine, Department of Biochemistry, Zonguldak, Turkey Phone: +90-372-2610169, Fax: +90-372-2610155,

References

1. Behçet H. Über residivierende Aphthose, durch ein Virus verursachte Geschwüre am Mund, am Auge und an den Genitalien. Dermatol Wochenschr 1937; 105:1152–7.Search in Google Scholar

2. Ghate JV, Jorizzo JL. Behçet's disease, and complex aphthosis. J Am Acad Dermatol 1999; 40:1–18.10.1016/S0190-9622(99)70523-2Search in Google Scholar

3. Sakane T, Takeno M, Suzuki N, Inaba G. Behcet's disease. N Engl J Med 1999; 341:1284–91.10.1056/NEJM199910213411707Search in Google Scholar

4. Hankey GJ, Eikelboom JW. Homocysteine and vascular disease. Lancet 1999; 354:407–13.10.1016/S0140-6736(98)11058-9Search in Google Scholar

5. Durand P, Prost M, Loreau N, Lussier-Cacan S, Blache D. Impaired homocysteine metabolism and atherothrombotic disease. Lab Invest 2001; 81:645–72.10.1038/labinvest.3780275Search in Google Scholar

6. Aviram M, Billecke S, Sorenson R, Bisgaier C, Newton R, Rosenbalt M, et al. Paraoxonase active site required for protection against LDL oxidation involves its free sulfhydryl group and is different from that required for its arylesterase/paraoxonase activities. Selective action of human paraoxonase allozymes Q and R. Arterioscler Thromb Vasc Biol 1998; 18:1617–24.10.1161/01.ATV.18.10.1617Search in Google Scholar

7. Niwa Y, Miyake S, Sakane T, Shingu M, Yokoyama M. Auto-oxidative damage in Behcet's disease – endothelial cell damage following the elevated oxygen radicals generated by stimulated neutrophils. Clin Exp Immunol 1982; 49:247–55.Search in Google Scholar

8. Takeno M, Kariyone A, Yamashita N. Excessive function of peripheral blood neutrophils from patients with Behcet's disease and from HLA B51 transgenic mice. Arthritis Rheum 1995; 38:426–33.10.1002/art.1780380321Search in Google Scholar

9. Kose K, Yazici C, Ascıoglu O. The evaluation of lipid peroxidation and adenosine deaminase activity in patients with Behcet's disease. Clin Biochem 2001; 34:125–9.10.1016/S0009-9120(01)00190-4Search in Google Scholar

10. Chambers JC, Haskard DO, Kooner JS. Vascular endothelial function and oxidative stress mechanisms in patients with Behcet's syndrome. J Am Coll Cardiol 2001; 37:517–20.10.1016/S0735-1097(00)01137-2Search in Google Scholar

11. Evereklioglu C. Current concepts in the etiology and treatment of Behcet disease. Surv Ophthalmol 2005; 50:297–350.10.1016/j.survophthal.2005.04.009Search in Google Scholar PubMed

12. Ozdemir R, Barutcu I, Sezgin AT, Acikgoz N, Ermis N, Metin Esen A, et al. Vascular endothelial function and plasma homocysteine levels in Behcet's disease. Am J Cardiol 2004; 94:522–5.10.1016/j.amjcard.2004.04.073Search in Google Scholar PubMed

13. Karakucuk S, Baskol G, Oner AO, Baskol M, Mirza E, Ustdal M. Serum paraoxonase activity is decreased in the active stage of Behcet's disease. Br J Ophthalmol 2004; 88:1256–8.10.1136/bjo.2004.043398Search in Google Scholar

14. International Study Group for Behcet's Disease. Criteria for diagnosis of Behcet's disease. Lancet 1990;335:1078–80.Search in Google Scholar

15. Hunter MI, Nlemadim BC, Davidson DI. Lipid peroxidation products and antioxidant proteins in plasma and cerebrospinal fluid from multiple sclerosis patients. Neurochem Res 1985; 10:1645–52.10.1007/BF00988606Search in Google Scholar

16. Gan KN, Smolen A, Eckerson HW, La Du BN. Purification of human serum paraoxonase/arylesterase: evidence for one esterase catalyzing both activities. Drug Metab Dispos 1991; 19:100–6.Search in Google Scholar

17. Erkilic K, Evereklioglu C, Cekmen M, Ozkiriş A, Duygulu F, Dogan H. Adenosine deaminase enzyme activity is increased and negatively correlates with catalase, superoxide dismutase and glutathione peroxidase in patients with Behcet's disease: original contributions/clinical and laboratory investigations. Mediators Inflamm 2003; 12:107–16.10.1080/0962935031000097754Search in Google Scholar

18. Kokcam I, Naziroglu M. Effects of vitamin E supplementation on blood antioxidants levels in patients with Behcet's disease. Clin Biochem 2002; 35:633–9.10.1016/S0009-9120(02)00400-9Search in Google Scholar

19. Kose K, Yazici C, Cambay N, Ascioglu O, Dogan P. Lipid peroxidation and erythrocyte antioxidant enzymes in patients with Behcet's disease. Tohoku J Exp Med 2002; 197:9–16.10.1620/tjem.197.9Search in Google Scholar

20. Geisel J, Hubner U, Bodis M, Schorr H, Knapp JP, Obeid R, et al. The role of genetic factors in the development of hyperhomocysteinemia. Clin Chem Lab Med 2003; 41:1427–34.10.1515/CCLM.2003.219Search in Google Scholar

21. Draper H, Hadley M. Malondialdehyde determination as index of lipid peroxidation. Methods Enzymol 1990; 186:421–31.10.1016/0076-6879(90)86135-ISearch in Google Scholar

22. Durrington PN, Mackness B, Mackness MI. Paraoxonase and atherosclerosis. Arterioscler Thromb Vasc Biol 2001; 21:473–80.10.1161/01.ATV.21.4.473Search in Google Scholar

23. Sanvanich P, Mackness B, Gaskell SJ, Durrington P, Mackness M. The effect of high-density lipoproteins on the formation of lipid/protein conjugates during in vitro oxidation of low-density lipoprotein. Biochem Biophys Res Commun 2003; 300:501–6.10.1016/S0006-291X(02)02849-8Search in Google Scholar

24. Aviram M, Hardak E, Vaya J, Mahmood S, Milo S, Hoffmann A, et al. Human serum paraoxonase (PON1) Q and R selectively decrease lipid peroxides in human coronary and carotid atherosclerotic lesions: PON1 esterase and peroxidase like activities. Circulation 2000; 101:2510–7.10.1161/01.CIR.101.21.2510Search in Google Scholar

25. Durand P, Prost M, Loreau N, Lussier-Cacan S, Blache D. Impaired homocysteine metabolism and atherothrombotic disease. Lab Invest 2001; 81:645–72.10.1038/labinvest.3780275Search in Google Scholar

26. Upchurch GR Jr, Welch GN, Fabian AJ, Freedman JE, Johnson JL, Keaney JF Jr, et al. Homocysteine decreases bioavailable nitric oxide by a mechanism involving glutathione peroxidase. J Biol Chem 1997; 272:17012–7.10.1074/jbc.272.27.17012Search in Google Scholar

27. Ates A, Aydıntug O, Olmez U, Duzgun N, Duman M. Serum homocysteine level is higher in Behcet's disease with vascular involvement. Rheumatol Int 2005; 25:42–4.10.1007/s00296-003-0398-9Search in Google Scholar

28. Canataroglu A, Tanriverdi K, Inal T, Seydaoglu G, Arslan D, Ozbek S, et al. Methylenetetrahydrofolate reductase gene C677T mutation and plasma homocysteine level in Behcet's disease. Rheumatol Int 2003; 23:236–40.10.1007/s00296-003-0301-8Search in Google Scholar

29. Evereklioglu C, Cumurcu T, Türköz Y, Özerol E, Sahin K, Doganay S. Serum homocysteine level is increased and correlated with endothelin-1 and nitric oxide in Behçet's disease. Br J Ophthalmol 2002; 86:653–7.10.1136/bjo.86.6.653Search in Google Scholar

30. Blacher J, Benetos A, Kirzin JM, Malmejac A, Guize L, Safar ME. Relation of plasma total homocysteine to cardiovascular mortality in a French population. Am J Cardiol 2002; 90:591–5.10.1016/S0002-9149(02)02561-4Search in Google Scholar

31. Stuart MJ. Platelet malonyldialdehyde formation: an indicator of platelet hyperfunction. Thromb Haemost 1979; 42:649–54.10.1055/s-0038-1666904Search in Google Scholar

32. Jakubowski H. Protein homocysteinylation: possible mechanism underlying pathological consequences of elevated homocysteine levels. FASEB J 1999; 13:2277–83.10.1096/fasebj.13.15.2277Search in Google Scholar

33. Jakubowski H. Homocysteine thiolactone and S-nitrosohomocysteine mediate incorporation of homocysteine into protein in humans. Clin Chem Lab Med 2003; 41:1462–6.10.1515/CCLM.2003.224Search in Google Scholar PubMed

34. Janel N, Robert K, Chabert C, Ledru A, Gouedard C, Barouki R, et al. Mouse liver paraoxonase-1 gene expression is downregulated in hyperhomocysteinemia. Thromb Haemost 2004; 92:221–2.10.1055/s-0037-1613648Search in Google Scholar

Received: 2006-2-6
Accepted: 2006-5-31
Published Online: 2006-9-8
Published in Print: 2006-9-1

©2006 by Walter de Gruyter Berlin New York

Articles in the same Issue

  1. Point-of-care testing – can we move from anecdote to evidence?
  2. A long and winding road: defining the biological role and clinical importance of paraoxonases
  3. Point-of-care testing in the cardiovascular operating theatre
  4. Low-density lipoprotein receptor-related protein 5 and vitamin D receptor gene polymorphisms in relation to vitamin D levels in menopause
  5. The methylenetetrahydrofolate reductase C677T gene mutation is associated with hyperhomocysteinemia, cardiovascular disease and plasma B-type natriuretic peptide levels in Korea
  6. Exploring allelic imbalance within paraffin-embedded tumor biopsies using pyrosequencing technology
  7. Detection of circulating tumour cells in blood by quantitative real-time RT-PCR: effect of pre-analytical time
  8. Hereditary hyper-ACE-emia due to the Pro1199Leu mutation of somatic ACE as a potential pitfall in diagnosis: a first family outside Europe
  9. Molecular assay for detection of the common carnitine palmitoyltransferase 1A 1436(C>T) mutation
  10. Serum cytokine levels and the expression of estrogen and progesterone receptors in breast cancer patients
  11. Protein Z levels and prognosis in patients with acute coronary syndromes
  12. Determination of total bilirubin in whole blood from neonates: results from a French multicenter study
  13. Analysis of protein S-100B in serum: a methodological study
  14. Lipid peroxidation and homocysteine levels in Behçet's disease
  15. Lower expression of the α2,3-sialylated fibronectin glycoform and appearance of the asialo-fibronectin glycoform are associated with high concentrations of fibronectin in human seminal plasma with abnormal semen parameters
  16. Automated processing of whole blood samples for the determination of immunosuppressants by liquid chromatography tandem-mass spectrometry
  17. Role of methionine residues of albumin in T-R conversion of hemoglobin
  18. Rheumatoid factor interference in the determination of carbohydrate antigen 19-9 (CA 19-9)
  19. Significance of Elecsys® S100 immunoassay for real-time assessment of traumatic brain damage in multiple trauma patients
  20. IFCC primary reference procedures for the measurement of catalytic activity concentrations of enzymes at 37°C: International Federation of Clinical Chemistry and Laboratory Medicine (IFCC): Scientific Division, Committee on Reference Systems for Enzymes (C-RSE): Part 8. Reference procedure for the measurement of catalytic concentration of α-amylase: [α-Amylase: 1,4-α-D-glucan 4-glucanohydrolase (AMY), EC 3.2.1.1]
  21. ESEAP: the national External Quality Assessment Scheme for clinical chemistry in Greece and Cyprus
  22. Evaluation of whole-genome amplification using multiple-displacement amplification of a limited number of cells
  23. Comparison of various methods for the determination of total protein in urine
  24. Description of examinations and their results and ISO standard 15189
  25. Congress of Clinical Chemistry and Laboratory Medicine, Annual Congress of the Society of Clinical Chemistry and Laboratory Medicine (DGKL) in association with The Austrian Society for Laboratory Medicine and Clinical Chemistry, The Swiss Society for Clinical Chemistry (SGKC), The German Association of Technical Assistants in Medicine (dvta), Mannheim, Germany, October 1st - 4th, 2006
  26. First Congress of the Austrian Society for Laboratory Medicine and Clinical Chemistry (ÖGLMKC), Salzburg, October 4 – 7, 2006
Downloaded on 8.11.2025 from https://www.degruyterbrill.com/document/doi/10.1515/CCLM.2006.191/html?lang=en
Scroll to top button