Serum oxidative stress status in CagA positive Helicobacter pylori infection

Abstract

Objectives: Previous studies have suggested that CagA positive Helicobacter pylori (H.pylori) infection may cause the various oxidative damages. The objective of this study was to investigate serum oxidative status in infectetion with CagA positive H.pylori strains. Materials and methods: Forty-two H.pylori CagA positive subjects and 39 H.pylori CagA negative subjects were enrolled. H.pylori infection was diagnosed by the histopathological assessment of gastric mucosa. CagA status was detected by enzyme immuno assay in a micro ELISA machine. Total antioxidant status (TAS) and total oxidant status (TOS) were measured autoanalyzer using commercially available kits. Serum oxidative stress index (OSI) was calculated using TAS and TOS measurements. Results: The levels TAS and TOS of CagA positive subjects were found to be 1.48 ± 0.18 mmol/L, 36.88 ± 19.84 mmol/L. Those of CagA negative group were measured to be 1.43 ± 0.19 mmol/L and 38.44 ± 14.72 mmol/L respectively. The values of serum OSI were similar (25.28 ± 15.85 and 26.48 ± 10.02) in CagA positive and negative groups. Conclusions: The measurements of serum oxidative status did not show any sigficant difference between the patients infected with CagA positive and CagA negative H.pilori strains.

Keywords

• Helicobacter pylori, CagA, oxidative status, total antioxidant status, total oxidant status, oxidative stress index.

CagA Pozitif Helikobakter pilori enfeksiyonunda serum oksidatif stres durumu

Öz

Amaç: Geçmişte Helikobakter pilori'nin değişik oksidatif hasarlara neden olabileceği gösterilmişti. Çalışmamızda H.pilori'nin CagA pozitif suşlarıyla enfekte hastalarda serum oksidatif durumu belirlemeyi amaçladık. Gereç ve yöntem: Çalışma H.pilori ile enfekte CagA pozitif 42, CagA negatif 39 hastada yürütüldü. H.pilori enfeksiyonu, mide biyopsilerinin histopatolojik değerledirmesi ile teşhis edildi. CagA durumu, enzim immuno assay yöntemiyle mikro ELISA cihazında belirlendi. Otoanalizör cihazında ticari kitleriyle serumda total antioksidan durum (TAS) ve total oksidan durum (TOS) ölçüldü, bulunan değerlerden serum oksidatif stres indeksi (OSI) hesaplandı. Bulgular: CagA pozitif grubun TAS, TOS ve OSI değerleri sırasıyla 1,48 ± 0,18 mmol/L, 36,88 ± 19,84 mmol/L ve 25,28 ± 15,85 bulundu. Negatif grubun verileri sırasıyla 1,43 ± 0,19 mmol/L, 38,44 ± 14,72 mmol/L, 26,48 ± 10,02 idi. Her iki grubun serum oksidatif duruma ilişkin parametreleri istatistikî olarak benzerdi. Sonuç: CagA pozitif ve CagA negatif suşlarla olan H.pilori enfeksiyonları arasında serum oksidatif durum parametreleri arasında anlamlı fark bulunamadı.

Anahtar Kelimeler

• Helikobakter pilori, CagA, oksidatif durum, total antioksidan durum, total oksidan durum, oksidatif stres indeksi.

References

1. Peek RM Jr. Helicobacter pylori strain-specific modulation of gastric mucosal cellular turnover: implications for carci- no-genesis. J Gastroenterol 2002;37(Suppl.13):10-6.
2. Hocker M, Hohenberger P. Helicobacter pylori virulence fac- tors - one part of a big picture. Lancet 2003;362(9391):1231- 33.
3. Minohara Y, Boyd DK, Hawkins HK, Ernst PB, Patel J, Crowe SE. The effect of the cag pathogenicity island on binding of Helicobacter pylori to gastric epithelial cells and the subsequent induction of apoptosis. Helicobacter 2007;12(6):583-90.
4. Niccoli G, Franceschi F, Cosentino N, et al. Coronary ath- erosclerotic burden in patients with infection by CagA- positive strains of Helicobacter pylori. Coron Artery Dis 2010;21(4):217-21.
5. Erel O. A novel automated method to measure total anti- oxidant response against potent free radical reactions. Clin Bio-chem 2004;37(2):112-9.
6. Aslan M, Nazligul Y, Horoz M, et al. Serum prolidase ac- tivity and oxidative status in Helicobacter pylori infection. Clin Biochem 2007;40(1-2):37-40.
7. Calabrese V, Guagliano E, Sapienza M, et al. Redox regu- lation of cellular stress response in aging and neurode- generative disorders: role of vitagenes. Neurochem Res 2007;32(4-5):757-73.
8. Rush JW, Denniss SG, Graham DA. Vascular nitric oxide and oxidative stress: determinants of endothelial adaptations to cardiovascular disease and to physical activity. Can J Appl Physiol 2005;30(4):442-74.

9. Takayanagi R, Inoguchi T, Ohnaka K. Clinical and experimen- tal evidence for oxidative stress as an exacerbating factor of diabetes mellitus. J Clin Biochem Nutr 2011;48(1):72-7.
10. Chang CS, Chen WN, Lin HH, Wu CC, Wang CJ. Increased oxidative DNA damage, inducible nitric oxide synthase, nuclear factor kappaB expression and enhanced antiapop- tosis-related proteins in Helicobacter pylori-infected non- cardiac gastric adenocarcinoma. World J Gastroenterol 2004;10(15):2232-40.
11. Kebapcilar L, Sari I, Renkal AH, et al. The influence of Helicobacter pylori eradication on leptin, soluble CD40 ligand, oxidative stress and body composition in patients with peptic ulcer disease. Intern Med 2009;48(24):2055-9.
12. Covacci A, Censini S, Bugnoli M, et al. Molecular charac- terization of the 128-kDa immunodominant antigen of He- lico-bacter pylori associated with cytotoxicity and duodenal ulcer. Proc Natl Acad Sci U S A 1993;90(12):5791-5.
13. Peters TM, Owen RJ, Slater E, Varea R, Teare EL, Sav- erymuttu S. Genetic diversity in the Helicobacter pylori cag pathogenicity island and effect on expression of anti- CagA serum antibody in UK patients with dyspepsia. J Clin Pathol 2001;54(3):219-23.
14. Gatti LL, Módena JL, Payão SL, et al. Prevalence of Heli- cobacter pylori cagA, iceA and babA2 alleles in Brazilian pa-tients with upper gastrointestinal diseases. Acta Trop 2006;10083):232-40.
15. Maeda S, Ogura K, Yoshida H, et al. Major virulence fac- tors, VacA and CagA, are commonly positive in Helico- bacter pylori isolates in Japan. Gut 1998;42(3):338-43.
16. Ching CK, Wong BC, Kwok E, Ong L, Covacci A, Lam SK. Prevalence of CagA-bearing Helicobacter pylori strains de-tected by the anti-CagA assay in patients with peptic ulcer disease and in controls. Am J Gastroenterol 1996;91(5):949-53.
17. Doğan E, Kefeli A, Nazlıgül Y, et al. Helicobakter pilori ile enfekte duodenal ülser ve fonksiyonel dispepsi hastalarında anti-cagA pozitifliği ve eradikasyon tedavi başarısına etkisi. Dicle Tıp Dergisi 2011;38(1):7-11.
18. Rudi J, Reuther S, Sieg A, Hoerner M, Stremmel W. Relıevance of underlying disease and bacterial vaca and caga status on the efficacy of Helicobacter pylori eradica- tion. Digestion 2002;65(1):11-15.
19. Eşrefoğlu M. Hücre hasarı ve ölümü: oksidatif stres ve an- tioksidan savunma sistemi Turkiye Klinikleri J Med Sci 2009;29(6):1660-76.
20. Hernández-Saavedra D, McCord JM. [Evolution and free radicals. Importance of oxidative stress in human pathol- ogy]. Rev Med Inst Mex Seguro Soc 2007;45(5):477-84.
21. Naito Y, Yoshikawa T. Molecular and cellular mechanisms involved in Helicobacter pylori-induced inflammation and oxidative stress. Free Radic Biol Med 2002;33(3):323-36.
22. Khodaii Z, Ghaderian SM, Akbarzadeh Najar R, Nejati H, Tabatabaei Panah AS. CagA and vacA status and influence of Helicobacter pylori infection on serum oxidative DNA damage in Iranian patients with peptic ulcer disease. Ir J Med Sci 2011;180(1):155-61.
23. Sun YQ, Girgensone I, Leanderson P, Petersson F, Borch K. Effects of antioxidant vitamin supplements on Helicobacter pylori-induced gastritis in Mongolian gerbils. Helicobacter 2005;10(1):33-42.
24. Farinati F, Della Libera G, Cardin R, et al. Gastric antioxi- dant, nitrites, and mucosal lipoperoxidation in chronic gas- tritis and Helicobacter pylori infection. J Clin Gastroenterol 1996;22(4):275-81.
25. Drake IM, Mapstone NP, Schorah CJ, et al. Reactive oxygen species activity and lipid peroxidation in Helicobacter py- lori associated gastritis: relation to gastric mucosal ascorbic acid concentrations and effect of H.pylori eradication. Gut 1998;4286:768-71.
26. Khanzode SS, Khanzode SD, Dakhale GN. Serum and plas- ma concentration of oxidant and antioxidants in patients of Helicobacter pylori gastritis and its correlation with gastric cancer. Cancer Lett 2003;195(1):27–31.
27. Li CQ, Pignatelli B, Ohshima H. Increased oxidative and nitrative stress in human stomach associated with cagA+ Helicobacter pylori infection and inflammation. Dig Dis Sci 2001;46(4):836-44.
28. Ladeira MS, Bueno RC, Dos Santos BF, et al. Relationship among oxidative DNA damage, gastric mucosal density and the relevance of cagA, vacA and iceA genotypes of He- licobacter pylori. Dig Dis Sci 2008;53(1):248-55.
29. Farinati F, Cardin R, Russo VM, Busatto G, Franco M, Rugge M. Helicobacter pylori CagA status, mucosal oxida- tive damage and gastritis phenotype: a potential pathway to cancer? Helicobacter 2003;8(3):227-34.
30. Tiwari SK, Manoj G, Sharma V, et al. Helicobacter pylori genotypes in gastric pathology and its association with plasma malondialdehyde and nitric oxide levels. Inflam- mopharmacology 2010;18(2):59-64.