Kronik böbrek hastalığı olan hastalarda oksidatif stress düzeyi

Year 2018, Volume: 10 Issue: 1, 45 - 50, 05.04.2018

İhsan Ateş , Nihal Özkayar Fatma Meriç Yılmaz , Nergiz Bayrakçı Salim Neselioğlu , Özcan Erel , Ezgi Coşkun Yenigün , Fatih Dede

https://doi.org/10.21601/ortadogutipdergisi.308443

Abstract

Amaç: Bu çalışmada kronik böbrek hastalığı olan hastalarda
dinamik tiyol/disülfid dengesinin araştırılması amaçlandı.

Gereç
ve Yöntem:  Çalışmaya evre 1-5 (non diyaliz)
150 (57 erkek, 93 kadın) kronik böbrek
hastası ve (76 (30 erkek, 46 kadın) sağlıklı
kontrol grubu alındı. Kan tiyol/disülfid dengesi yeni geliştirilen otomatik ve
kalorimetrik bir yöntemle ölçüldü.

Bulgular: Tüm
popülasyonun serum thiol düzeyi ortalaması 320.8±57.8 µmol/L, total
thiol düzeyi ortalaması 352.0±61.5 µmol/L, ortalama disülfid düzeyi 15.6±5.3 µmol/L idi.
Kronik böbrek hastalarında ortalama serum thiol (p<0.001), total thiol (p<0.001) ve disülfid düzeyleri (p<0.001) kontrol grubuna kıyasla
anlamlı olarak daha düşüktü.  Kronik
böbrek hastaları ve kontrol grubu arasında disülfid/thiol, disülfid/total tihol
ve thiol /total thiol oranları açısından olarak anlamlı
farklılık saptanmadı.

Sonuç: Çalışamızda hem tiyol hem disülfid düzeyinde azalma
olması Kronik böbrek hastalarında serum tiyol düşüklüğünün
sadece tiyol gruplarının disülfide çevrimine değil, vücuttaki total tiyol
rezervinin azalmasına da bağlı olduğunu göstermektedir. Bu nedenle kronik böbrek hastalığında tiyol rezervini attırmaya yönelik nutrisyonel destek sağlanması
önerilebilir. 

Keywords

: Merkaptanlar, oksidatif stres, sülfidril, tiyol oksidasyonu, üremi

Oxidative stress level in patients with chronic kidney disease

Abstract

Background: In this study, we aimed to evaluate the presence of
oxidative stress in chronic kidney disease (CKD) by measuring dynamic thiol/disulphide homeostasis.

Material and Method: A
hundred fifty patients (57 men, 93 women) followed with a diagnosis of CKD
(stages 1-5, not on dialysis) and 76 healthy, disease-free individuals (30 men,
46 women) were included in the study. Blood thiol/disulphide homeostasis was
measured by newly developed automatic and colorimetric method by Erel and Neselioglu.

Results: The mean serum native thiol (p =
0.001), total thiol (p = 0.001) and disulphide (p =
0.041) levels were lower in CKD than in the control group. No significant
difference was found between the CKD and control groups in terms of disulphide/thiol, disulphide/total
thiol and thiol/total thiol ratios (p >
0.05). Serum native thiol and total thiol levels
were correlated negatively with both BMI and serum phosphorous level while both
the parameters were correlated positively with glomerular filtration rate,
total protein level and albumin level. A negative correlation was found between
total thiol and age. Disulphide
levels were correlated positively with albumin and total protein and negatively
with uric acid levels.

Conclusion: Our study shows that low serum thiol
levels in CKD is due to a decrease in total thiol reserve of the body and not
due to conversion of thiol groups into disulphides. 

Keywords

Mercaptans, oxidative stress, sulfhydryl, thiol oxidation, uremia

References

• Referans 1. Hallan SI, Coresh J, Astor BC, Asberg A, Powe NR, Romundstad S et al. International comparison of the relationship of chronic kidney disease prevalence and ESRD risk. Journal of the American Society of Nephrology : JASN. 2006;17(8):2275-84. doi:10.1681/ASN.2005121273.
• Referans 2. Massy ZA, Stenvinkel P, Drueke TB. The role of oxidative stress in chronic kidney disease. Seminars in dialysis. 2009;22(4):405-8. doi:10.1111/j.1525-139X.2009.00590.x.
• Referans 3. Dounousi E, Papavasiliou E, Makedou A, Ioannou K, Katopodis KP, Tselepis A et al. Oxidative stress is progressively enhanced with advancing stages of CKD. American journal of kidney diseases : the official journal of the National Kidney Foundation. 2006;48(5):752-60. doi:10.1053/j.ajkd.2006.08.015.
• Referans 4. Sugamura K, Keaney JF, Jr. Reactive oxygen species in cardiovascular disease. Free radical biology & medicine. 2011;51(5):978-92. doi:10.1016/j.freeradbiomed.2011.05.004.
• Referans 5. McCord JM. Human disease, free radicals, and the oxidant/antioxidant balance. Clinical biochemistry. 1993;26(5):351-7.
• Referans 6. Filomeni G, Rotilio G, Ciriolo MR. Cell signalling and the glutathione redox system. Biochemical pharmacology. 2002;64(5-6):1057-64.
• Referans 7. Prakash M, Upadhya S, Prabhu R. Protein thiol oxidation and lipid peroxidation in patients with uraemia. Scandinavian journal of clinical and laboratory investigation. 2004;64(6):599-604. doi:10.1080/00365510410002869.
• Referans 8. Erel O, Neselioglu S. A novel and automated assay for thiol/disulphide homeostasis. Clinical biochemistry. 2014;47(18):326-32. doi:10.1016/j.clinbiochem.2014.09.026.
• Referans 9. Miyata T, Sugiyama S, Saito A, Kurokawa K. Reactive carbonyl compounds related uremic toxicity ("carbonyl stress"). Kidney international Supplement. 2001;78:S25-31. doi:10.1046/j.1523-1755.2001.59780025.x.
• Referans 10. Clermont G, Lecour S, Lahet J, Siohan P, Vergely C, Chevet D et al. Alteration in plasma antioxidant capacities in chronic renal failure and hemodialysis patients: a possible explanation for the increased cardiovascular risk in these patients. Cardiovascular research. 2000;47(3):618-23.
• Referans 11. Himmelfarb J, McMonagle E, McMenamin E. Plasma protein thiol oxidation and carbonyl formation in chronic renal failure. Kidney international. 2000;58(6):2571-8. doi:10.1046/j.1523-1755.2000.00443.x.
• Referans 12. Levey AS, Eckardt KU, Tsukamoto Y, Levin A, Coresh J, Rossert J et al. Definition and classification of chronic kidney disease: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney international. 2005;67(6):2089-100. doi:10.1111/j.1523-1755.2005.00365.x.
• Referans 13. Levey AS, Stevens LA, Schmid CH, Zhang YL, Castro AF, 3rd, Feldman HI et al. A new equation to estimate glomerular filtration rate. Annals of internal medicine. 2009;150(9):604-12.
• Referans 14. Ziegler DM. Role of reversible oxidation-reduction of enzyme thiols-disulfides in metabolic regulation. Annual review of biochemistry. 1985;54:305-29. doi:10.1146/annurev.bi.54.070185.001513.
• Referans 15. Himmelfarb J, McMonagle E. Albumin is the major plasma protein target of oxidant stress in uremia. Kidney international. 2001;60(1):358-63. doi:10.1046/j.1523-1755.2001.00807.x.
• Referans 16. Hu ML. Measurement of protein thiol groups and glutathione in plasma. Methods in enzymology. 1994;233:380-5.
• Referans 17. Davies KJ, Sevanian A, Muakkassah-Kelly SF, Hochstein P. Uric acid-iron ion complexes. A new aspect of the antioxidant functions of uric acid. The Biochemical journal. 1986;235(3):747-54.
• Referans 18. Narasimhan S, Gokulakrishnan K, Sampathkumar R, Farooq S, Ravikumar R, Mohan V et al. Oxidative stress is independently associated with non-alcoholic fatty liver disease (NAFLD) in subjects with and without type 2 diabetes. Clinical biochemistry. 2010;43(10-11):815-21. doi:10.1016/j.clinbiochem.2010.04.003.
• Referans 19. Ross EA, Koo LC, Moberly JB. Low whole blood and erythrocyte levels of glutathione in hemodialysis and peritoneal dialysis patients. American journal of kidney diseases : the official journal of the National Kidney Foundation. 1997;30(4):489-94.
• Referans 20. Deneke SM. Thiol-based antioxidants. Current topics in cellular regulation. 2000;36:151-80.
• Referans 21. Agarwal R, Vasavada N, Sachs NG, Chase S. Oxidative stress and renal injury with intravenous iron in patients with chronic kidney disease. Kidney international. 2004;65(6):2279-89. doi:10.1111/j.1523-1755.2004.00648.x.
• Referans 22. Tepel M, van der Giet M, Statz M, Jankowski J, Zidek W. The antioxidant acetylcysteine reduces cardiovascular events in patients with end-stage renal failure: a randomized, controlled trial. Circulation. 2003;107(7):992-5.