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Number of results
2011 | 65 | 4 | 63–69

Article title

Stres oksydacyjny – reaktywne formy tlenu i azotu w patogenezie zaburzeń układu krążenia

Content

Title variants

EN
Oxidative stress – reactive oxygen and nitrogen species in the pathogenesis of cardiovascular disorders

Languages of publication

PL

Abstracts

PL
Powstawanie reaktywnych form tlenu i azotu jest częścią prawidłowych przemian biochemicznych i w warunkach fizjologicznych podlega ścisłej kontroli przez system licznych mechanizmów antyoksydacyjnych. W warunkach patologicznych dochodzi jednak do zwiększenia generowania zarówno wolnych rodników, jak i nierodnikowych czynników utleniających, co przewyższa możliwości obrony antoksydacyjnej organizmu. Pojawiający się stres oksydacyjny prowadzi do nieodwracalnych uszkodzeń komórek i tkanek. Wiadomo, że reaktywne formy tlenu i azotu są zaangażowane w rozwój wielu zaburzeń związanych z układem sercowo-naczyniowym, takich jak miażdżyca, nadciśnienie, cukrzyca czy uszkodzenia związane z niedokrwieniem serca i reperfuzją. Prezentowana praca stanowi krótki przegląd dostępnych danych, dotyczących biochemicznych podstaw udziału stresu oksydacyjnego w patogenezie i rozwoju wybranych chorób układu sercowo-naczyniowego.
EN
The generation of reactive oxygen and nitrogen species is a part of normal metabolism and under physiological conditions undergoes a strict control by a variety of enzymatic and non-enzymatic anti-oxidative mechanisms. However, under pathological conditions, the enhanced production of free radicals and non-radical oxidants may be overwhelm the anti-oxidative defence, leading to oxidative stress and irreversible damage of cells and tissues. It has been established, that increased production of reactive oxygen and nitrogen species has been implicated in the development of cardiovascular system-related disorders, including hypertension, atherosclerosis, diabetes, and ischemia-reperfusion injury. The presented review is a brief insight on the role of oxidative stress in the pathogenesis and progression of cardiovascular diseases, related to haemostasis disturbances and endothelium dysfunction.

Discipline

Year

Volume

65

Issue

4

Pages

63–69

Physical description

Contributors

  • Katedra Biochemii Ogólnej Uniwersytetu Łódzkiego ul. Pomorska 141/143 90-236 Łódź tel. 42 635 44 82 e-mail: joannak@biol.
author
  • Katedra Biochemii Ogólnej Uniwersytetu Łódzkiego
  • Katedra Biochemii Ogólnej Uniwersytetu Łódzkiego

References

  • 1. Bartosz G. Druga twarz tlenu. Wydawnictwo Naukowe PWN 2003: 144–226.
  • 2. Dhalla N.S., Elmoselhi A.B., Hata T., Makino N. Status of myocardial antioxidants in ischemia-reperfusion injury. Cardiovasc. Res. 2000; 47: 446–456.
  • 3. Förstermann U. Oxidative stress in vascular disease: causes, defense mechanisms and potential therapies. Nat. Clin. Pract. Cardiovasc. Med. 2008; 5: 338–349.
  • 4. Pacher P., Beckman J.S., Liaudent L. Nitric oxide and peroxynitrite in health and disease. Physiol. Rev. 2007; 87: 315–324.
  • 5. Kołodziejczyk J. 3-nitrotyrozyna – marker stresu oksydacyjnego in vitro i in vivo. Diagn. Lab. 2010; 2: 141–145.
  • 6. Nowak P., Olas B., Wachowicz B. Stres oksydacyjny w przebiegu hemostazy. Post. Bioch. 2010; 3: 239–247.
  • 7. Levi M., van der Poll T. Two-way interactions between infl ammation and coagulation. Trends Cardiovasc. Med. 2005; 15: 254–259.
  • 8. Aird W.C. The role of the endothelium in severe sepsis and multiple organ dysfunction syndrome. Blood 2003; 101: 3765–3777.
  • 9. Madamanchi N.R., Vendrov A., Rune M.S. Oxidative stress and vascular disease. Arterioscler. Thromb. Vasc. Biol. 2005; 25: 29–38.
  • 10. Cai H., Harrison D.G. Endothelial dysfunction in cardiovascular diseases. Circ. Res. 2000; 87: 840–844.
  • 11. Weseler A.R., Bast A. Oxidative stress and vascular function: implications for pharmacologic treatments. Curr. Hypertens. Rep. 2010; 12: 154–161.
  • 12. Förstermann U. Nitric oxide and oxidative stress in vascular disease. Pfl ugers Arch. – Eur. J. Physiol. 2010; 459: 923–929.
  • 13. Coleman J.W. Nitric oxide in immunity and infl ammation. Int. Immunopharmacol. 2001; 1: 1397–1406.
  • 14. Lufrano M., Balazy M. Interaction of peroxynitrite and other nitrating substances with human platelets: the role of glutathione and peroxynitrite permeability. Biochem. Pharmacol. 2003; 65: 515–523.
  • 15. Ronson R.S., Nakamura M., Vinten-Johansen J. The cardiovascular eff ects and implications of peroxynitrite. Cardiovasc. Res. 1999; 44: 47–59.
  • 16. Schopfer F.J., Baker P.R.S., Feeman B.A. NO-dependent protein nitration: a cell signaling event or an oxidative infl ammatory response? Trends Biochem. Sci. 2003; 28: 646–654.
  • 17. Krötz F., Sohn H.Y., Pohl U.L. Reactive oxygen species. Players in the platelet game. Arterioscler. Thromb. Vasc. Biol. 2004; 24: 1988–1996.
  • 18. Santilli F., Basili S., Ferroni P., Davě G. CD40/CD40L system and vascular disease. Intern. Emerg. Med. 2007; 2: 256–258.
  • 19. Prontera C., Martelli N., Evangelista V. i wsp. Homocysteine modulates the CD40/ CD40L system. J. Am. Coll. Cardiol. 2007; 49: 2182–2210.
  • 20. Andre P., Nannizzi-Alimo L., Prasad S.K. Platelet-derived CD40L: the switch-hitting player of cardiovascular disease. Circulation 2002; 106: 896–899.
  • 21. Landmesser U., Dikalov S., Price S.R. i wsp. Oxidation of tetrahydrobiopterin leads to uncoupling of endothelial cell nitric oxide synthase in hypertension. J. Clin. Invest. 2003; 111: 1201–1209.
  • 22. Yokoyama M. Oxidative stress and atherosclerosis. Curr. Opin. Pharmacol. 2004; 4: 110–115.
  • 23. Grieve D.J., Byrne J.A., Cave A.C., Shah A.M. Role of oxidative stress in cardiac remodeling after myocardial infraction. Heart Lung Circ. 2004; 13: 132–138.
  • 24. Pacher P., Schulz R., Liaudet L., Szabó C. Nitrosative stress and pharmacological modulation of heart failure. Trends Pharmacol. Sci. 2005; 26: 302–310.
  • 25. Sucu N., Unlü A., Tamer L. i wsp. 3-nitrotyrosine in atherosclerotic blood vessels. Clin. Chem. Lab. Med. 2003; 41(1): 23–35.
  • 26. Zou M.H., Leist M., Ullrich U. Selective nitration of prostacyclin synthase and defective vasorelaxation in atherosclerotic bovine coronary arteries. Am. J. Path. 1999; 154: 1359–1365.
  • 27. Lancel S., Tissier S., Mordon S., i wsp. Peroxynitrite decomposition catalysts prevent myocardial dysfunction and infl ammation in endotoxemic rats. J. Am. Coll. Cardiol. 2004; 12: 2348–2358.
  • 28. Griendling K.K., FitzGerald G.A. Oxidative stress and cardiovascular injury. Circulation 2003; 108: 1912–1916.
  • 29. Matsunaga T., Nakajima T., Sonoda M., i wsp. Modulation of reactive oxygen species in endothelial cells by peroxynitritetreated lipoproteins. J. Biochem. 2001; 130: 285–293.
  • 30. Racz A., Veresh Z., Lotz G., Bagi Z., Koller A. Cyclooxygenase-2 derived thromboxane A2 and reactive oxygen species mediate fl ow-induced constrictions of venules in hyperhomocysteinemia. Atherosclerosis 2010; 208: 43–49.
  • 31. Vadseth C., Souza J.M., Thomson L. i wsp. Pro-thrombotic state induced by post-translational modifi cation of fi brinogen by reactive nitrogen species. J. Biol. Chem. 2004; 279: 8820–8826.
  • 32. Nowak P., Wachowicz B. Peroxynitritemediated modifi cation of fi brinogen aff ects platelet aggregation and adhesion. Platelets 2002; 13: 293–299.
  • 33. Nowak P., Żbikowska H.M., Ponczek M. i wsp. Diff erent vulnerability of fi brinogen subunits to oxidative/nitrative modifi cations induced by peroxynitrite: functional consequences. Thromb. Res. 2007; 121: 163–174.
  • 34. Nowak P., Wachowicz B. Studies on pig blood platelet responses to peroxynitrite action. Platelets 2001; 12: 376–381.
  • 35. Nowak P., Olas B., Bald E. i wsp. Peroxynitrite- induced changes of thiol groups in human blood platelets. Platelets 2003; 14(6): 375–379.
  • 36. Pignatelli B., Li C.Q., Boff etta P. i wsp. Nitrated and oxidized plasma proteins in smokers and lung cancer patients. Cancer Res. 2001; 61: 778–784.
  • 37. Nowak P., Kołodziejczyk J., Wachowicz B. Peroxynitrite and fi brinolytic system; the eff ect of peroxynitrite on plasmin activity. Mol. Cell. Bioch. 2004; 267: 141–146.
  • 38. Hathuc C., Hermo R., Schulze J., Gugliucci A.. Nitration of human plasminogen by RAW 264.7 macrophages reduces streptokinase-induced plasmin activity. Clin. Chem. Lab. Med. 2006; 44: 213– –219.
  • 39. Gugliucci A. Human plasminogen is highly susceptible to peroxynitrite inactivation. Clin. Chem. Lab. Med. 2003; 41(8): 1064–1068.
  • 40. Wożakowska-Kapłon B., Bartkowiak R., Stępień A. Zespół metaboliczny – epidemia naszych czasów, nowa defi nicja, cele działań prewencyjnych i leczniczych. Przew. Lek. 2005; 6: 32–38.
  • 41. Roberts C.K., Barnard R.J., Sindhu R.K., Jurczak M., Ehdaie A., Vaziri N.D. Oxidative stress and dysregulation of NAD(P)H oxidase and antioxidant enzymes in dietinduced metabolic syndrome. Metabolism 2006; 55: 928–934.
  • 42. Vincent H.K., Taylor A.G. Biomarkers and potential mechanisms of obesity induced oxidant stress in humans. Int. J. Obes. 2006; 30: 400–408.
  • 43. Keany F., Larson M.G., Vasan R.S. i wsp. Obesity and systemic oxidative stress: clinical correlates of oxidative stress in the Framingham study. Arterioscler. Thromb. Vasc. Biol. 2003; 23: 434–439.
  • 44. Funder J.W. Is aldosterone bad for the heart? Trends Endocrinol. Metab. 2004; 15: 139–142.
  • 45. Skřtt O., Uhrenholt T.R., Schjerning J., Hansen P.B., Rasmussen L.E., Jensen B.L. Rapid actions of aldosterone in vascular health and disease – friend or foe? Pharmacol. Ther. 2006; 111: 495–507.
  • 46. Ceriello A., Mercuri F., Quagliaro L. i wsp. Detection of nitrotyrosine in the diabetic plasma: evidence of oxidative stress. Diabetologia 2001; 44: 834–838.
  • 47. Kesavulu M.M., Giri R., Kameswara Rao B., Apparao C. Lipid peroxidation and antioxidant enzyme levels in type 2 diabetics with microvascular complications. Diabetes Metab. 2000; 26: 387–392.
  • 48. Brownlee M. Biochemistry and molecular cell biology of diabetic complications. Nature 2001; 414: 813–820.
  • 49. Kaneto H., Matsuoka T.A., Nakatani Y. i wsp. Oxidative stress, ER stress, and the JNK pathway in type II diabetes. J. Mol. Med. 2005; 83: 429–439.

Document Type

article

Publication order reference

Identifiers

YADDA identifier

bwmeta1.element.psjd-c45d932e-5005-4cbc-861f-43d9ca6bd5d1
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