ZNAČAJ POLIMORFIZAMA REGULATORNIH I KATALITIČKIH ANTIOKSIDANTNIH PROTEINA U HRONIČNOJ BUBREŽNOJ SLABOSTI
Ključne reči:
HBS, Nrf2, SOD2, GPX1, genski polimorfizmi
Sažetak
Hroničnu bubrežnu slabost (HBS) karakterišu prekomerno stvaranje slobodnih radikala i smanjenje antioksidantne zaštite. Stoga, razlike u individualnoj podložnosti HBS mogu ležati u funkcionalnim varijacijama gena koji kodiraju regulatorne i katalitičke antioksidantne proteine, poput Nrf2, superoksid dizmutaze (SOD) i glutation peroksidaze (GPX). Identifikovano je više različitih polimorfizma u okviru gena koje kodiraju ove enzime, poput Nrf2(-617C/A), SOD2(Ala16Val) and GPX1(Pro198Leu) koji dovode do promena u njihovoj aktivnosti. Do sada najmanje ispitan polimorfizam od navedenih u podložnosti, progresiji bolesti i preživljavanju u HBS je Nrf2(-617C/A) polimorfizam. Rezultati dve studije koje su ispitivale navedeni polimorfizam ukazaju da ne postoji individualna povezanost ovog polimorfizma sa rizikom za nastanak terminalne bubrežne slabosti (TBS), oksidativnim fenotipom, niti preživljavanjem. S druge strane, Nrf2 je imao značajan uticaj na rizik za nastanak TBS i preživljavanje u kombinaciji sa polimorfizmima drugih antioksidantnih gena. Rezultati istraživanja koji se odnose na povezanost SOD2(Ala16Val) i GPX1(Pro198Leu) polimorfizama i HBS su kontradiktorni. S jedne strane, pokazano je da pacijenti nosioci manje aktivnih SOD2(Val) ili GPX1(Leu) alela imaju veći rizik za razvoj i progresiju HBS. Ipak, druge studije ukazuju na odustvo povezanosti ovih polimorfizama sa HBS. Rezultati jedinog istraživanja u kome je ispitivana povezanost GPX1 polimorfizma i preživljavanja (ukupnog i kardiovaskularnog) kod pacijenata sa TBS, su pokazali značajan uticaj GPX1(Leu/Leu) genotipa na duže preživljavanje. Rezultati prikazani u ovom radu mogu biti od značaja kako bi se dale preporuke za dalja klinička i translaciona istraživanja. Razvoj istraživanja u oblasti polimorfizama antioksidantnih gena kod pacijenata sa HBS-om može doprineti boljoj stratifikaciji ovih pacijenata na osnovu panela antioksidantnih gena. Takav panel bi mogao da bude dalje korišćen u kontekstu predviđanja preživljavanja CKD pacijenata, što bi takođe doprinelo razvijanju personalizovanog pristupa u lečenju pacijenata, uključujući primenu ciljane antioksidantne terapije.
Reference
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3. Tonelli M, Wiebe N, Culleton B, House A, Rabbat C, Fok M, et al. Chronic kidney disease and mortality risk: a systematic review. J Am Soc Nephrol. 2006;17(7):2034–47.
4. Thompson S, James M, Wiebe N, Hemmelgarn B, Manns B, Klarenbach S, et al. Cause of death in patients with reduced kidney function. J Am Soc Nephrol. 2015;26(10):2504–11.
5. Fiorillo C, Oliviero C, Rizzuti G, Nediani C, Pacini A, Nassi P. Oxidative stress and antioxidant defenses in renal patients receiving regular haemodialysis. Clin Chem Lab Med. 1998;36(3):149–53.
6. Vaziri ND. Oxidative stress in uremia: nature, mechanisms, and potential consequences. In: Seminars in nephrology. Elsevier; 2004. p. 469–73.
7. Himmelfarb J, Stenvinkel P, Ikizler TA, Hakim RM. The elephant in uremia: oxidant stress as a unifying concept of cardiovascular disease in uremia. Kidney Int. 2002;62(5):1524–38.
8. Oberg BP, Mcmenamin E, Lucas FL, Mcmonagle E, Morrow J, Ikizler TA, et al. Increased prevalence of oxidant stress and inflammation in patients with moderate to severe chronic kidney disease. Kidney Int. 2004 Mar;65(3):1009–16.
9. Vaziri ND, Oveisi F, Ding Y. Role of increased oxygen free radical activity in the pathogenesis of uremic hypertension. Kidney Int. 1998;53(6):1748–54.
10. Sies H. Oxidative stress: from basic research to clinical application. Am J Med. 1991;91(3):S31–8.
11. Sies H. Oxidative stress: eustress and distress in redox homeostasis. In: Stress: physiology, biochemistry, and pathology. Elsevier; 2019. p. 153–63.
12. Massy ZA, Ceballos I, Chadefaux-Vekemens B, Nguyen-Khoa T, Descamps-Latscha B, Drüeke TB, et al. Homocyst (e) ine, oxidative stress, and endothelium function in uremic patients. Kidney Int. 2001;59(S78):S243.
13. Malhotra JD, Kaufman RJ. Endoplasmic reticulum stress and oxidative stress: a vicious cycle or a double-edged sword? Antioxid Redox Signal. 2007;9(12):2277–94.
14. Chin MP, Reisman SA, Bakris GL, O’grady M, Linde PG, McCullough PA, et al. Mechanisms contributing to adverse cardiovascular events in patients with type 2 diabetes mellitus and stage 4 chronic kidney disease treated with bardoxolone methyl. Am J Nephrol. 2014;39(6):499–508.
15. Ward RA, McLeish KR. Polymorphonuclear leukocyte oxidative burst is enhanced in patients with chronic renal insufficiency. J Am Soc Nephrol. 1995;5(9):1697–702.
16. Galvan DL, Green NH, Danesh FR. The hallmarks of mitochondrial dysfunction in chronic kidney disease. Kidney Int. 2017;92(5):1051–7.
17. Laher I. Systems biology of free radicals and antioxidants. Springer; 2014.
18. Nguyen AT, Lethias C, Zingraff J, Herbelin A, Naret C, Descamps-Latscha B. Hemodialysis membrane-induced activation of phagocyte oxidative metabolism detected in vivo and in vitro within microamounts of whole blood. Kidney Int. 1985;28(2):158–67.
19. Tbahriti HF, Kaddous A, Bouchenak M, Mekki K. Effect of different stages of chronic kidney disease and renal replacement therapies on oxidant-antioxidant balance in uremic patients. Biochem Res Int. 2013;2013.
20. Girelli D, Olivieri O, Stanzial AM, Azzini M, Lupo A, Bernich P, et al. Low platelet glutathione peroxidase activity and serum selenium concentration in patients with chronic renal failure: relations to dialysis treatments, diet and cardiovascular complications. Clin Sci. 1993;84(6):611–7.
21. Ceballos-Picot I, Witko-Sarsat V, Merad-Boudia M, Nguyen AT, Thévenin M, Jaudon MC, et al. Glutathione antioxidant system as a marker of oxidative stress in chronic renal failure. Free Radic Biol Med. 1996;21(6):845–53.
22. Sung C-C, Hsu Y-C, Chen C-C, Lin Y-F, Wu C-C. Oxidative stress and nucleic acid oxidation in patients with chronic kidney disease. Oxid Med Cell Longev. 2013;2013.
23. Daenen K, Andries A, Mekahli D, Van Schepdael A, Jouret F, Bammens B. Oxidative stress in chronic kidney disease. Pediatr Nephrol. 2019;34(6):975–91.
24. Ward RA, Ouseph R, Mcleish KR. Effects of high-flux hemodialysis on oxidant stress. Kidney Int. 2003;63(1):353–9.
25. Jankowska M, Rutkowski B, Dębska-Ślizień A. Vitamins and microelement bioavailability in different stages of chronic kidney disease. Nutrients. 2017;9(3):282.
26. Davies KJ. Protein damage and degradation by oxygen radicals. I. general aspects. J Biol Chem. 1987;262(20):9895–901.
27. Wolff SP, Garner A, Dean RT. Free radicals, lipids and protein degradation. Trends Biochem Sci. 1986;11(1):27–31.
28. Imlay JA, Linn S. DNA damage and oxygen radical toxicity. Science (80- ). 1988;240(4857):1302–9.
29. Mimić-Oka J, Savić-Radojević A, Plješa-Ercegovac M, Opačić M, Simić T, Dimković N, et al. Evaluation of oxidative stress after repeated intravenous iron supplementation. Ren Fail. 2005;27(3):345–51.
30. Choi B, Kang K-S, Kwak M-K. Effect of redox modulating NRF2 activators on chronic kidney disease. Molecules. 2014;19(8):12727–59.
31. Tucker PS, Dalbo VJ, Han T, Kingsley MI. Clinical and research markers of oxidative stress in chronic kidney disease. Biomarkers. 2013;18(2):103–15.
32. Grieve DJ, Pljesa-Ercegovac M, Savic-Radojevic A, Damjanovic T, Dimkovic N, McClements L, et al. Research Article GSTM1 Modulates Expression of Endothelial Adhesion Molecules in Uremic Milieu. 2021;
33. Marzec JM, Christie JD, Reddy SP, Jedlicka AE, Vuong H, Lanken PN, et al. Functional polymorphisms in the transcription factor NRF2 in humans increase the risk of acute lung injury. FASEB J. 2007;21(9):2237–46.
34. Sutton A, Khoury H, Prip-Buus C, Cepanec C, Pessayre D, Degoul F. The Ala16Val genetic dimorphism modulates the import of human manganese superoxide dismutase into rat liver mitochondria. Pharmacogenet Genomics. 2003;13(3):145–57.
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