medigraphic.com

2016, Número 1

Siguiente >>

Rev Fac Med UNAM 2016; 59 (1)


Especies reactivas de oxígeno, sepsis y teoría metabólica del choque séptico

Carrillo ER, Díaz Ponce MJA, Peña PCA, Flores ROI, Neri MR, Zepeda MAD, Pérez CÁA, Ortiz TA

Idioma: Español
Referencias bibliográficas: 41
Paginas: 6-18
Archivo PDF: 1113.73 Kb.


RESUMEN

La sepsis es una de las principales causas de mortalidad en la unidad de terapia intensiva. El término especies reactivas de oxígeno (ERO) incluye moléculas con un electrón impar, llamadas radicales libres, como el anión superóxido, y también agentes oxidados como el peróxido de hidrógeno. Las ERO pueden reaccionar con muchas moléculas y pueden producir un daño no controlado; sin embargo, también tienen un papel fundamental en el metabolismo celular.
El estrés oxidante es el resultado de la respuesta inflamatoria asociada a la sepsis que produce cambios en la función mitocondrial y en la microcirculación. El objetivo de este trabajo es revisar el papel de las ERO en sepsis y nuevos conceptos relacionados con la teoría metabólica del choque séptico.


REFERENCIAS (EN ESTE ARTÍCULO)

  1. Schorr C, Zanotti S, Dellinger P. Severe sepsis and septic shock. Management and performance improvement. Virulence. 2014;5:190-99.

  2. Carrillo-Esper R, Carrillo-Córdova JR, Carrillo-Córdova LD. Estudio epidemiológico de la sepsis en unidades de terapia intensiva mexicanas. Cirugía y Cirujanos. 2009; 77:301-8.

  3. Goldenberg NM, Steinberg BE, Slutsky AS, Lee WL. Broken barriers: a new take on sepsis pathogenesis. Sci Transl Med. 2011;3:88-125.

  4. Xiao W, Mindrinos MN, Seok J, Cuschieri J, Cuenca AG, Gao H, Hayden DL, Hennessy L, Moore EE, et a l. A genomic storm in critically injured humans. J Exp Med. 2011;208:2581-90.

  5. Nduka OO, Parrillo JE. The pathophysiology of septic shock. Crit Care Clin. 2009;25(4):677-702.

  6. Pravda J. Metabolic theory of septic shock. World J Crit Care Med. 2014;3:45-54.

  7. Le Bras M, Clement MV, Pervaiz S, Brenner C. Reactive oxygen species and the mitochondrial signaling pathway of cell death. Histol Histopathol. 2005;20:205-20.

  8. Apel K, Hirt H. Reactive Oxygen Species: Metabolism, Oxidative Stress, and Signal Transduction. Annu Rev Plant Biol. 2004;55:373-99.

  9. Valko M, Morris H, Cronin M. Metals, toxicity and oxidative stress. Current Medicinal Chemistry. 2005;12:1161- 208.

  10. Cadenas E, Sies H. The lag phase. Free Radical Research. 1998;28:601-9.

  11. Halliwell B. Reactive oxygen species in living systems: Source, biochemistry and role in human disease. Am J Med. 1991;91:14-22.

  12. Lambeth JD. Nox/Duox family of nicotinamide adenine dinucleotide (phosphate) oxidases. Current Opinion in Hematology. 2002;9:11-17.

  13. Antunes F, Cadenas E. Estimation of H2O2 gradients across biomembranes. FEBS Letters. 2000;475:121-6.

  14. Pastor N, Weinstein H, Jamison E, Brenowitz M. A detailed interpretation of OH radical footprints in a TBP DNA complex reveals the role of dynamics in the mechanism of sequence specific binding. Journal of Molecular. Biology. 2000;304:55-68.

  15. Leonard SS, Harris GK, Shi X . Metal induced oxidative stress and signal transduction. Free Radical Biology and Medicine. 2004;37:1921-42.

  16. Liochev SI, Fridovich I. The Haber-Weiss cycle–70 years later: An alternative view. Redox Report. 2002;7:55-7.

  17. Duma D, Fernandes D, Bonini MG, Stadler K, Mason RP, et al. NOS-1-derived NO is an essential triggering signal for the development of systemic inflammatory responses. European Journal of Pharmacology. 2011; 668:285-92.

  18. Cadenas E. Basic mechanisms of antioxidant activity. Biofactors. 1997;6:391-7.

  19. Kumar H, Kawai T, Akira S. Pathogen recognition by the innate immune system. Int Rev Immunol. 2011;30:16-34.

  20. Medzhitov R. Origin and physiological roles of inflammation. Nature. 2008;454:428-35.

  21. Crimi E, Sica V, Williams-Ignarro S, Zhang H, Slutsky AS, Ignarro LJ, Napoli C. The role of oxidative stress in adult critical care. Free Radic Biol Med. 2006;40:398-406.

  22. Volk T, Kox WJ. Endothelium function in sepsis. Inflamm Res 2000; 49: 185-198.

  23. Bernal ME, Varon J, Acosta P, Montagnier L. Oxidative stress in critical care medicine. Int J Clin Pract. 2010; 64:1480-8.

  24. Shumer W, Gupta TK, Moss GS, Nyhus L. Effect of endotoxemia on liver cell mitochondria in man. Ann Surg. 1970; 171:875-82.

  25. Callahan LA, Stofan DA, Szweda LI, Nethery DE, Supinski GS. Free radicals alter maximal diaphragmatic mitochondrial oxygen consumption in endotoxin induced sepsis. Free Radic Biol Med. 2001;30:129-38.

  26. Boveris A, Alvarez S, Navarro A. The role of mitochondrial nitric oxide synthase in inflammation and septic shock. Free Radic Biol Med. 2002;33:1186-93.

  27. Svistunenko DA, Davies N, Brealey D, Singer M, Cooper CE. Mitochondrial dysfunction in patients with severe sepsis: an EPR interrogation of individual respiratory chain components. Biochim Biophys Acta. 2006;1757:262-72.

  28. Salvemini D, Cuzzocrea S. Oxidative stress in septic shock and disseminated intravascular coagulation. Free Radic Biol Med. 2002;33: 1173-85.

  29. Macarthur H, Westfall TC, Riley, Misko TP, Salvemini D. Inactivation of catecholamines by superoxide gives new insights on the pathogenesis of septic shock. Proc Natl Acad Sci. 2000;97:9753-8.

  30. Motoyama T, Okamoto K, Kukita I , Hamaguchi M, Kinoshita Y, Ogawa H. Possible role of increased oxidant stress in multiple organ failure after systemic inflammatory response syndrome. Crit Care Med. 2003;31:1048-52.

  31. Luchtemberg MN, Petronilho F, Constantino L , Gelain DP, Andrades M, Ritter C, et al. Xanthine oxidase activity in patients with sepsis. Clin Biochem 2008;41:1186- 90.

  32. Kirkeboen KA, Strand OA. The Role of nitric oxide in sepsis- an overview. Acta Anaesthesiol Scand. 1999;43:275-88.

  33. Parratt JR. Nitric oxide. A key mediator in sepsis and endotoxaemia. J Physiol Pharmacol. 1997;48:493-506.

  34. Cuzzocrea S, Riley DP, Caputi AP, Salvemini D. Antioxidant therapy: a new pharmacological approach in shock, inflammation, and ischemia/reperfusion injury. Pharmacol Rev. 2001;53:135-59.

  35. Szabo C. Nitric oxide, peroxynitrite and poly (ADP-Ribose) synthase: biochemistry and pathophysiological implications. En: Rubanyi GM (ed). Pathophysiology and clinical application of nitric oxide. Harwood, NJ: Academic Publishers; 1999. pp 69-98.

  36. American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Me. 20;1992:864-74.

  37. Phelps DT, Ferro TJ, Higgins PJ, Shankar R, Parker DM, Johnson A. TNF-alpha induces peroxynitrite-mediated depletion of lung endothelial glutathione via protein kinase C. Am. J. Physiol. 1995;269:L551-9.

  38. Bindoli A, Deeble DJ, Rigobello MP, Galzigna L. Direct and respiratory chain-mediated redox cycling of adrenochrome. Biochim Biophys Acta. 1990;1016:349-56.

  39. Forman HJ, Zhang H, Rinna A. Glutathione: overview of its protective roles, measurement, and biosynthesis. Mol Aspects Med. 2009;30:1-12.

  40. Rahman I, Biswas SK. Noninvasive biomarkers of oxidative stress: reproducibility and methodological issues. Redox Rep. 2004;9:125-43.

  41. Salvemini D, Wang ZQ, Stern MK, Currie MG, Misko TB. Peroxynitrite decomposition catalysts: therapeutics for peroxynitrite-mediated pathology. Proc Natl Acad Sci USA. 1998;95:2659-63.




2020     |     www.medigraphic.com