Paraoxonase activities and erythrocyte TBARS levels in patients with Behçet’s disease and recurrent aphthous stomatitis

Amaç: Bu çalışmanın amacı Behçet hastaları ve rekküren aftöz stomatitli (RAS) hastalarda antioksidan enzimlerden süperoksid dismutaz (SOD), katalaz (CAT) ve paraoksonaz (PON1) ile lipid peroksidasyonunu gösteren tiyobarbitürik asidle ilişkili substrat (TBARS) düzeyleri yanı sıra 192. pozisyonda paraoksonaz fenotipini belirleyerek, hem Behçet ile rekküren aftöz stomatitli hastalarda antioksidan enzimlerin durumunu tespit etmek hem de 192. pozisyonda paraoksonaz fenotipinin Behçet Hastalığına bir yatkınlık yaratıp yaratmadığını belirlemektir. Gereç ve Yöntem: Bu amaçla 25 Behçet hastası, 27 RAS’li hasta ile 45 sağlıklı gönüllü çalışmaya dahil edilmiştir. Eritrosit SOD, CAT, PON1 enzim aktiviteleri ve TBARS düzeyi spektrofotometrik olarak, 192. pozisyonda PON1 fenotipi Eckersonun önerdiği PON1 histogram antimode kullanılarak belirlenmiştir. Bulgular: Eritrosit TBARS ve SOD enzim aktiviteleri Behçet hastalarında kontrole göre anlamlı yüksek bulunmuştur (p=0.05). Kolşisin tedavisi alan Behçet hastalarında (n=10) TBARS düzeyleri düşerken, antioksidan enzimlerde bir değişiklik gözlenmedi. Behçet hastalarının %18’i, kontrollerin %13,6’sı BB fenotipi taşıyordu. Sonuç: Kolşisin tedavisinin eritrosit TBARS düzeylerini düşürmesi nedeniyle, Behçet hastalığının patofizyolojisinde polimorfnükleer lökositlerin serbest radikallerin temel kaynağını oluşturmaktadır. Ayrıca çalışmamız BB alleli taşıyan olguların Behçet Hastalığına yatkınlığının daha fazla olabileceğini gösteren bir ön çalışma niteliğindedir. Ancak olgu sayısının arttırılarak bu konuda daha ileri çalışmalara gereksinim bulunmaktadır.

Behçet hastalığı ve rekkürren aftöz stomatitli hastalarda paraoksonaz aktivitesi ve eritrosit TBARS düzeyleri

Aim: The aim of our study is to evaluate paraoxonase (PON1), superoxide dismutase (SOD) and catalase (CAT) activities which is antioxidant enzymes, and tiobarbituric acid substance (TBARS) levels, one of the end products of lipid peroxidation induced by reactive oxygen species, in patients with Behçet’s disease (BD) and Recurrent Aphthous Stomatitis. We also aimed to investigate if paraoxonase phenotyping at position 192., may prone to affect to prone to Behcet’s disease and Recurrent Aphthous Stomatitis or not. Materials and Methods: Eryrocyte SOD, CAT activities and TBARS levels, serum PON1 activities were measured by using spectrophotometer. Individuals were classified for PON1 phenotype using the antimode of histogram of PON1 as proposed by Eckerson. Results: Erytrocyte TBARS levels and SOD activities of Behcet’s disease group higher than controls (p=0.05). While TBARS levels depleted in patients under treatment with colchicines, no effect was observed on the antioxidant enzyme activities by colchicine treatment in Behcet’s disease patients (n=10). We also investigated if paraoxonase phenotyping affected to prone to Behcet’s disease. While 18% of patients with Behcet’s disease had BB phenotype, 13,6% of controls. Conclusion: Although our data can not exactly indicate that B allele carriers are more prone to BD and/or any chronic inflammatory disease, taking into account this preliminary study with limited number of cases, we can propose that B allele carriers may have a tendency for these diseases, and further population studies on this allele frequency related with these diseases are needed.

___

  • 1. International study group for Behçet’s disease, criteria for diagnosis of Behçet’s disease. Lancet 1990;335:1078-1080.
  • 2. Whallett AJ, Thurairajan G, Hamburger J, et al. Behçet’s syndrome: A multidisciplinary approach to clinical care. Q J Med 1999;92:727-740.
  • 3. Pronai L, Ichikawa Y, Nakazawa H, Arimori S. Enhanced superoxide generation and the decreased superoxide scavenging activity of peripheral blood leucocytes in Behçet’s disease-effects of colchicine. Clin Exp Rheumatol 1991;9(3):227-233.
  • 4. Köse K, Dogan P, Ascioglu M, et al. Oxidative stress and antioxidant defences in plasma of patients with Behçet’s disease. Tohoku J Exp med 1995;176(4):239-248.
  • 5. Dogan P, Tanrıkulu G, Soyuer U, Kose K. Oxidative enzymes of polymorphonuclear leukocytes and plasma fibrinogen, ceruloplasmin and copper levels in Behçet’s disease. Clin Biochem 1994;27(5):413-418.
  • 6. Freitas JP, Filipe P, Yousefi A, et al. Oxidative stress in Adamantiades-Behçet’s disease. Dermatology 1998; 197(4): 343-348.
  • 7. Kim Y, Greenberg MS. Management of patients with severe oral mucosal disease. Alpha Omegan, 2001;94:18-23
  • 8. Pugliese PT. The skin’s antioxidant systems. Dermatol Nursing 1998;10:401–416.
  • 9. Halliwell B. Reactive oxygen species in living system: source, biochemistry, and role in human disease. Am J Med 1991;91(Suppl 3C):14–22.
  • 10. Goswami B, Tayal D. Gupta N, Mallika V. Paraoxonase: A multifaceted biomolecule Clinica Chimica Acta 2009;410:1–12.
  • 11. Adkins S, Gan KN, Mody M, La Du BN. Molecular basis for the polymorphic forms of human serum paraoxonase/arylesterase: Glutamine or arginine at position 192, for the respective A or B allozymes. Am J Hum Genet 1993;52(3):598-608.
  • 12. Azarsız E, Sözmen EY. Paraoksonaz ve klinik önemi. Türk Biyokimya Dergisi 2000;3:109-119.
  • 13. La Du BN, Aviram M, Billecke S, et al. On the physiological role(s) of the paraoxonases. Chem Biol Interact 1999;(14):379-388.
  • 14. Karakucuk S, Baskol G, Oner AO, Baskol M, Mirza E, Ustdal M. Serum paraoxonase activity is decreased in the active stage of Behçet’s disease. Br J Ophthalmol 2004;88:1256-1258.
  • 15. Sozmen EY, Tanyalçın T, Kutay F, Onat T. Ethanol induced oxidative stress and membrane injury in rats. Eur J Clin Chem Clin Biochem 1994;32:741-744.
  • 16. Sozmen B, Delen Y, Girgin FK, Sözmen EY. Catalase and paraoxonase activities in hypertensive type2DM; correlation with glycemıc control.Clin Biochem 1999;32(6):423-427.
  • 17. Eckerson HW, Wyte C, La Du BN. The human serum paraoxonase/arylsterase polymorphism. Am J Hum Genet 1983;35:1126-1138.
  • 18. Kose K, Yazici C, Cambay N, et al. Lipid peroxidation and erythrocyte antioxidant enzymes in patients with Behçet’s disease. Tohoku J Exp Med 2002;197:9-16.
  • 19. Mackness B, Durrington PN, Mackness MI. Human serum paraoxonases. Gen Pharm 1998;31(3):329-336.
  • 20. Ayub A, Mackness MI, Arrol S, et al. Serum paraoxonases after myocardial infarction. Arterioscler Thromb Vasc Biol 1999;19:330-335.
  • 21. Mackness MI, Harty D, Bhatnaga D, et al. Serum paraoxonase activity in familial hypercholesterolemia and insulin-dependent diabetes mellitus. Atherosclerosis 1991;86:193-199.
  • 22. Levinsky RJ, Lehner T. Circulating immune complexes in Behçet’s syndrome and recurrent oral ulcers. J Lab Clin Med 1981;97:559-564.
  • 23. Whicher J, Biasucci L, Rifai N. Inflammation, the acute phase response and atherosclerosis. Clin Chem Lab Med 1999;37(5):495-503.
  • 24. Ruiz J, Blanche H, James RW, et al. Gln-Arg192 polymorphism of paraoxonase and coronary heart disease in type 2 diabetes. Lancet 1995;346;869-872.
  • 25. Hegele RA, Connelly PW, Scherer SW, et al. Paraoxonase-2 gene (PON2) G148 variant associated with elevated fasting plasma glucose in noninsulin-dependent diabetes mellitus. J Clin Endocrinol Metab 1997;82(10):3373-3377.
  • 26. Mackness B, Mackness MI, Durrington PN, et al. Paraxonase activity in two healthy populations with differing rates of coronary heart disease. Eur J Clin Invest 2000;30:4-10.
  • 27. Sanghera DK, Saha N, Aston CE, Kamboh MI. Genetic polymorphism of paraoxonase and the risk of coronary heart disease. Arterioscler Thromb Vasc Biol 1997;17:1067-1073.
Ege Tıp Dergisi-Cover
  • ISSN: 1016-9113
  • Yayın Aralığı: Yılda 4 Sayı
  • Başlangıç: 1962
  • Yayıncı: Ersin HACIOĞLU