Relationship between Helicobacter pylori and thiol-disulfide homeostasis: A prospective observational study

Year 2020, Volume: 5 Issue: 2, 38 - 42, 31.08.2020

Umut Eren Erdogdu , Hacı Çaycı , Ali Tardu , Ufuk Arslan , Yasemin Üstündağ , Özcan Erel , Hakan Demirci , Hasan Çantay

https://doi.org/10.25000/acem.635688

Abstract

Aim: Helicobacter pylori (HP) infection
causes inflammation and oxidative stress at a cellular level. In the present
study, we aimed to evaluate the possible relationship between HP and thiol-disulfide
homeostasis (TDH), a novel indicator of oxidative stress.

Methods: Medical
data of a total of 53 patients admitted with persistent dyspepsia and
undergoing gastroscopy were evaluated prospectively. The patients were divided
into two groups, based on the result of gastric biopsy, as HP-positive (+) and
HP-negative (-). Demographic data, ferric-reducing ability of plasma (FRAP),
ischemia-modified albumin (IMA), native thiol, total thiol, disulfide, and
malondialdehyde (MDA) levels of the patients were recorded and compared between
the two groups.

Results: The
native thiol (451.03 mmol/L vs. 407.03mmol/L, p=0.005) and total thiol (493.20
mmol/L vs. 456.40 mmol/L, p=0.027) levels were significantly higher in the HP
(+) group than in the HP (-) group. The disulfide levels and disulfide/native
thiol, disulfide/total thiol and native thiol/total thiol ratios were similar between
the HP (+) and HP (-) groups. Although the FRAP was lower in the HP (+) group
than in the HP (-) group, this difference was not statistically significant
(0.94 mmol/L vs. 1.10 mmol/L). No statistically significant difference was
found between the groups in the IMA and MDA levels.

Conclusion: In this study, oxidative status of HP patients was
evaluated in several different methods. Among them, only elevated native thiol
and total thiol levels were found in HP-induced gastritis. There is a need for
further studies involving a larger number of patients and a subgroup analysis
to examine whether elevated serum thiol-disulfide levels in HP infection
suggest an antioxidant or pro-oxidant status.

Keywords

Helicobacter pylori, homeostasis, thiol, disulfide, oxidative stress

Helicobacter pylori ve tiyol-disülfid homeostazı arasındaki ilişki: Prospektif, gözlemsel bir çalışma

Abstract

Amaç: Helicobacter pylori (HP)
enfeksiyonu, hücresel düzeyde inflamasyona ve oksidatif strese neden olur. Bu
çalışmada, oksidatif stresin bir göstergesi olan tiyol-disülfid homeostazı
(TDH) ve HP arasındaki olası ilişkiyi değerlendirmeyi amaçladık.

Yöntemler: Dispepsi yakınması ile başvuran
ve gastroskopi uygulanan toplam 53 hastanın tıbbi verileri prospektif olarak değerlendirildi.
Hastalar gastrik biyopsi sonucuna göre HP-pozitif (+) ve HP-negatif (-) olarak iki
gruba ayrıldı. Hastaların demografik verileri, plazma ferik indirgeme kabiliyeti
(FRAP), iskemi modifiye albümin (IMA), native tiyol, total tiyol, disülfid ve malondialdehit
(MDA) düzeyleri kaydedildi ve iki grup arasında karşılaştırıldı.

Bulgular: Doğal tiyol (451,03 mmol/L ve
407.03 mmol/L, p=0.005) ve toplam tiyol (493.20 mmol/L ve 456.40 mmol/L, p=0,027)
seviyeleri HP (+) grubunda HP (-) grubuna göre anlamlı olarak daha yüksekti.
Disülfid düzeyleri ve disülfid / native thiol, disülfid/total tiyol ve native
tiyol / total tiyol oranları HP (+) ve HP (-) grupları arasında benzerdi. FRAP,
HP (+) grubunda HP (-) grubuna göre daha düşük olmasına rağmen, bu fark
istatistiksel olarak anlamlı değildi (0,94 mmol/L ve 1,10 mmol/L). IMA ve MDA
düzeylerinde gruplar arasında istatistiksel olarak anlamlı bir fark saptanmadı.

Sonuç: HP kaynaklı gastrit gibi
oksidatif stresin arttığı koşullar altında serum tiyol-disülfid düzeylerinin
yükselmesi görülebilir. HP enfeksiyonunda yüksek serum tiyol-disülfid
düzeylerinin antioksidan veya pro-oksidan durumu gösterip göstermediğini
incelemek için daha fazla sayıda hasta ve alt grup analizi içeren çalışmalara
ihtiyaç vardır.

Keywords

Helicobacter pylori, homeostaz, tiyol, disülfid, oksidatif stres

References

• 1. Wroblewski LE, Peek RM Jr, Wilson KT. Helicobacter pylori and gastric cancer: factors that modulate disease risk. Clin Microbiol Rev. 2010;23:713-39.
• 2. Jiang, J, Chen Y, Shi, J, Song C, Zhang J, Wang, K. Population attributable burden of Helicobacter pylori-related gastric cancer, coronary heart disease, and ischemic stroke in China. Eur J Clin Microbiol Infect Dis. 2017;36:199-212.
• 3. McColl KE. Helicobacter pylori infection. N Engl J Med. 2010, 29;362:1597-604.
• 4. Helicobacter and Cancer Collaborative Group. Gastric cancer and Helicobacter pylori: a combined analysis of 12 case control studies nested within prospective cohorts. Gut, 2001,49: 347-53.
• 5. Butcher LD, den Hartog G, Ernst PB, Crowe SE. Oxidative Stress Resulting From Helicobacter pyloriInfection Contributes to Gastric Carcinogenesis. Cell Mol Gastroenterol Hepatol. 2017,20;3:316-22.
• 6. Bar-Or D, Lau E, Rao N, Bampos N, Winkler JV, Curtis CG. Reduction in the cobalt binding capacity of human albumin with myocardial ischemia. Ann Emerg Med, 1999, 34:S56.
• 7. Ustundag Y, Huysal K, Kahvecioglu S, Demirci H, Yavuz S, Sambel M, et al. Establishing reference values and evaluation of an in-house ferric reducing antioxidant power (FRAP) colorimetric assay in microplates. Eur Res J, 2016;2:126-31.
• 8. Drake IM, Mapstone NP, Schorah CJ, White KL, Chalmers DM, Dixon MF, et al. Reactive oxygen species activity and lipid peroxidation in Helicobacter pylori associated gastritis: relation to gastric mucosal ascorbic acid concentrations and effect of H pylori eradication. Gut. 1998;42:768-71.
• 9. Hansen RE, Roth D, Winther JR. Quantifying the global cellular thiol–disulfide status. Proc Natl Acad Sci U S A. 2009;106:422-7.
• 10. Amagase K, Nakamura E, Endo T, Hayashi S, Hasumura M, Uneyama H et al. New Frontiers in Gut Nutrient Sensor Research: Prophylactic Effect of Glutamine Against Helicobacter pylori–Induced Gastric Diseases in Mongolian Gerbils. J Pharmacol Sci. 2010;112:25-32.
• 11. Handa O, Naito Y, Yoshikawa T. Helicobacter pylori: a ROS-inducing bacterial species in the stomach. Inflamm Res. 2010;59:997-1003.
• 12. Aslan M, Nazligul Y, Horoz M, Bolukbas C, Bolukbas FF, Aksoy N, et al. Serum prolidase activity and oxidative status in Helicobacter pylori infection. Clin Biochem. 2007;40:37-40.
• 13. Erel O, Neselioglu, S. A novel and automated assay for thiol/disulphide homeostasis. Clin Biochem. 2014;47:326-32.
• 14. Hagag AA, Amin SM, El-Fiky RB, El-Sayad ME. Study of serum levels of some oxidative stress markers in children with Helicobacter pylori infection. Infect Disord Drug Targets. 2018;18:52-9.
• 15. Cichota LC, Moresco RN, Duarte MM, da Silva JE. Evaluation of ischemia‐modified albumin in anemia associated to chronic kidney disease. J Clin Lab Anal. 2008;22:1-5.
• 16. Duarte MM, Rocha JB, Moresco RN, Duarte T, Da Cruz IB, Loro VL, et al. Association between ischemia-modified albumin, lipids and inflammation biomarkers in patients with hypercholesterolemia. Clin Biochem. 2009;42:666-71.
• 17. Kaefer M, Piva SJ, De Carvalho JA, Da Silva DB, Becker AM, Coelho AC, et al. Association between ischemia modified albumin, inflammation and hyperglycemia in type 2 diabetes mellitus. Clin Biochem. 2010;43:450-4.
• 18. Başyiğit S, Akbaş H, Süleymanlar İ, Kemaloğlu D, Koç S, Süleymanlar G. The assessment of carotid intima-media thickness, lipid profiles and oxidative stress markers in Helicobacter pylori-positive subjects. Turk J Gastroenterol. 2012;23:646-51.
• 19. Halliwell B. Free radicals, antioxidants, and human disease: curiosity, cause, or consequence? Lancet. 1994, 10;344:721-4.
• 20. Ghezzi P, Bonetto V, Fratelli M. Thiol–disulfide balance: from the concept of oxidative stress to that of redox regulation. Antioxid Redox Signal. 2005;7:964-72.
• 21. Atmaca G. Antioxidant effects of sulfur-containing amino acids. Yonsei Med J. 2004;45:776-88.
• 22. Lynch SM, Campione AL, Moore MK. Plasma thiols inhibit hemin-dependent oxidation of human low-density lipoprotein. Biochim Biophys Acta. 2000;1485:11-22.
• 23. Naja F, Kreiger N, McKeown Eyssen G, Allard J. Bioavailability of vitamins E and C: does H. pylori infection play a role? Ann Nutr Metab. 2010;56:253-9.
• 24. Baykan AR, Biçer C, Gerçeker E, Erel Ö, Cerrah S, Albayrak B, et al. Thiol/disulphide homeostasis in Helicobacter pylori infected patients. European Res J. 2019;5:948-56.