¿Las especies reactivas del oxígeno y el sistema de defensa antioxidante se relacionan con la respuesta inflamatoria del SARS-CoV-2?
DOI:
https://doi.org/10.56050/01205498.1622Palabras clave:
Especies reactivas del oxígeno, estrés oxidativo, SARS-Cov-2, citoquinasResumen
El nuevo coronavirus SARS-CoV-2 también conocido como 2019-nCoV ocasiona la COVID-19, continúa siendo desconocido para el mundo de la salud por los cambios genómicos, fenotípicos del virus y los cambios fisiopatológicos relacionados con la respuesta proinflamatoria y procoagulante que genera en el huésped y su alta mortalidad. En la literatura médica, el aumento de las especies reactivas del oxígeno o radicales libres de oxígeno se asocia con la respuesta inflamatoria secundaria a la infección por virus y bacterias con el consecuente daño celular, tisular y sistémico en el huésped. La acción prooxidativa celular del virus SARS-CoV-2 hace que se pierda la hemostasia redox, que aumenten las especies reactivas del oxígeno y se genere estrés oxidativo con pérdida de la función del sistema antioxidante. Conocer la relación que tienen las especies reactivas del oxígeno y el sistema de defensa antioxidante con la respuesta inflamatoria del SARS-CoV-2, ayudará a entender e interpretar mejor la COVID-19.
Se realizó una revisión sistemática de la literatura médica a través de las bases de datos de PubMed y Medline con los términos: Infección por SARS-CoV-2, especies reactivas del oxígeno en la COVID-19, respuesta inflamatoria en la COVID-19.
Esta revisión mostró relación de la infección, inflamación, coagulación con el aumento de las especies reactivas del oxígeno y la pérdida del sistema de defensa antioxidante en la respuesta inflamatoria al SARS-CoV-2.
Biografía del autor/a
Rubén Darío Camargo Rubio, AMCI - Asociación Colombiana de Medicina Crítica y Cuidado Intensivo
Médico especialista en Medicina Interna; subespecialista en Cuidado Intensivo. Maestría en Gestión de Trasplantes. Maestría en Bioética. Miembro correspondiente Academia Nacional de Medicina, Capítulo Atlántico. Coordinador sección de Bioética y gestión de trasplantes AMCI 2020.
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40. Li YR., Jia Z., Trush MA. Defining ROS in Biology and Medicine. React Oxyg Species (Apex). 2016;1(1):9-21.
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53. Panfoli I. Potential role of ectopic redox complexes on the surface of endothelial cells in the pathogenesis of COVID-19 disease. Clin Med. 2020;20(5):e146-e147.
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58. Foley J.H., Conway E.M. Cross talk pathways between coagulation and inflammation. Circ Res. 2016;118(9):1392–408.
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3. Moran JF, James EK, Rubio MC, Sarath G, Klucas RV, Becana M. Functional Characterization and Expression of a Cytosolic Iron-Superoxide Dismutase from Cow- pea (Vigna unguiculata) Root Nodules. Plant Physiol. 2003;(133):773-782.
4.Piña-Garza E., Radicales Libres Beneficios y problemas (simposios). Gaceta Médica de México. [Internet].1996 [consultado 08 de mayo de 2021];132(2):183-203. Disponible en:
https://www.anmm.org.mx/bgmm/1864_2007/1996- 132-2-183-203.pdf
5. Finkel T, Holbrook N.J. Oxidants, oxidative stress and the biology of ageing. Nature. 2000; 408(6809):239–247.
6. FJ. Hurtado Breddaa, N. Nin Vaezab, H. Rubbo Amoninic. Estrés oxidativo y nitrosativo en la sepsis. Med Inten- siva.2005;29(3):159-65.
7. Apel K., Hirt H. Reactive oxygen species: Metabolism, oxidative stress, and signal transduction. Annu. Rev. Plant Biol. 2004;55:373–399.
8. McCord, J.M. The evolution of free radicals and oxidative stress. Am. J. Med. 2000;108(8): 652–659.
9. Lowenstein CJ, Dinerman JL, Snyder SH. Nitric Oxide:APhysiologic Messenger. Ann lntern Med. 1994;120(3):227- 237.
10. Mittler, R. Oxidative stress, antioxidants and stress toler ance. Trends Plant Sci.2002;7(9):405–410.
11. Pedraza-Chaverri J., Cárdenas-Rodríguez N., Chirino YI. El óxido nítrico y las especies reactivas de nitrógeno. Aspectos básicos e importancia biológica. Educación Química. 2006;17(4):443-451.
12. Expósito LA, Kokoszka JE, Waymire KG. Mitochondrial oxidative stress in mice lacking the glutatione peroxidase-1 gene. Free Radic Biol Med. 2000;28(5):754-66.
13. Armone-Caruso A., Del Prete A., Lazzarino AI., Expósito LA, Kokoszka JE, Waymire KG. Mitochondrial oxidative stress in mice lacking the glutatione peroxidase-1 gene. Free Radic Biol Med. 2000;28(5):754-66.
14. Market M, Andrew PC, Babior BM. Measurement of O2- production by human neutrophils. The preparation and assay of NADPH oxidase-containing particles from human neutrophils. Methods Enzimol 1984;105:358-65.
15. Coronado M., Vega S., Rey L., Vázquez M., Radilla C. Antioxidantes: Perspectiva actual para la salud humana. Rev. Chil. Nutr. 2015;42(2):206-212.
16. Borut P., Dušan Š.Milisav I. Achieving the balance be- tween ROS and antioxidants: when to use the synthetic antioxidants. Oxid Med Cell Longev. 2013;2013: 956792.
17. Mayor-Oxilia, R. Estrés Oxidativo y Sistema de Defensa Antioxidante. Rev. Inst. Med. Trop. 2010;5(2):23-29.
18. Fridovich I. Superóxido dismutasas. Annu Rev Biocem. 1975;44:147-159.
19. Arch. Bioechem Biophyns. 1984;228(2):617-620.
20. Rodríguez-Perón JM., Menéndez-Lopez JR., Trujillo-Lopez Y. Radicales libres en la biomedicine y estrés oxidativo. Rev Cub Med Mil. 2001;30(1):15-20.
21. Mittler, R. Oxidative stress, antioxidants and stress tolerance. Trends Plant Sci. 2002;7(8): 405–410.
22. Eiserich, J.P., van der Vliet, A., Handeltman, GJ., Halliwell. B. Cross, C.E. Antioxidantes dietéticos y daño biomole- cular inducido por el humo del cigarrillo: una interacción compleja. Am. J. Clin. Nutr.1995;62(6):1490S-1500S.
23. Montero M. Los radicales libres y las defensas antioxidantes. Revisión. AnalFacMed Univ Nal Mayor de San Marcos.1996;57(4); 278-281.
24. Segurola-Gurrutxaga H., Cárdenas-Lagranja G., Bur- gos-Peláez R. Nutrientes e inmunidad. Nutr Clin Med 2016;X(1):1-19.
25. Li, X., Geng, M., Peng Y., Meng Y. Lu S. Molecular im- mune pathogenesis and diagnosis of COVID-19. X. Li et al., Molecular immune pathogenesis and diagnosis of COVID-19. J Pharm Anal. 2020;10(2):102–108.
26. Lu R., Zhao X., Li J., Ni P., Yang B., Wu H., et al. Genomic caracterisation and epidemiology of 2019 novel corona- virus: implications for virus origins and receptor binding. Lancet. 2020;395(10224):565 – 574.
27. Mousavizadeh, L., Ghasemi S. Genotype and phenotype of COVID-19: Their roles in pathogenesis. J. Microbiol. Immunol. Infec. 202154(2):159-163.
28. Chen Y., Liu Q., Guo D. Emerging coronaviruses: Genome structure, replication, and pathogenesis. J. Med. Virol.2020;92:418- 23.
29. Letko M, Marzi A, Munster V. Functional assessment of cell entry and receptor usage for SARS-CoV-2 and other lineage B betacoronaviruses. Nat Microbiol. 2020;5:562-569.
30. Hoffmann M, Weber HK, Schroeder S, Krüger Herrler T, Erichsen S. et al. SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a 1clinically-proven protease inhibitor. Cell. 2020;181(2):271-289.
31. Song W, Gui M, Wang X, Xiang Y. Cryo-EM structure of the SARS coronavirus spike glycoprotein in complex with its host cell receptor ACE2. PLoS Pathog. 2018;14(8):e1007236.
32. Hao, X.; Liang, Z.; Jiaxin, D.; Jiakuan, P.; Hongxia, D.; Xin, Z. et al. High expression of ACE2 receptor of 2019 nCoV on the epithelial cells of oral mucosa. Int. J. Oral Sci. 2020;12(1):8.
33. Eakachai, P., Chutitorn K., Tanapat P. Immune responses in COVID-19 and potential vaccines: Lessons learned from SARS and MERS epidemic. Asian Pac. J. Allergy Immunol. 2020;38(1):1-9.
34. Li G., Fan Y., Lai Y, Han T., Li Z., Zhou P., et al. Coronavirus infections and immune responses. J Med Virol. 2020;92(4):424-432.
35. Gralinski LE, Sheahan TP, Morrison TE, et al. Complement activation contributes to severe acute respiratory syndrome coronavirus pathogenesis. mBio. 2018;9(5):e01753‐18.
36. Rokni, M.; Ghasemi, V. & Tavakoli, Z. Immune responses and pathogenesis of SARS-CoV-2 during an outbreak in Iran: Comparison with SARS and MERS. Rev Med Virol. 2020;30(3):e2107.
37. Lopez PGT, Ramírez SMLP, Torres AMS. Participantes de la respuesta inmunológica ante la infección por SARS- CoV-2. Alerg Asma Inmunol Pediatr. 2020;29(1):5-15.
38. Haipeng Z., Ti W. CD4+T, CD8+T counts and severe COVID-19: A meta-analysis J Infect.2020;81 (3):e82–e84.
39. Guan W, Ni Z.,Hu Y., Liang W.,Ou C., He J., et al. Clinical Characteristics of Coronavirus Disease 2019 in China. N Engl J Med. 2020;382(18):1708-1720.
40. Li YR., Jia Z., Trush MA. Defining ROS in Biology and Medicine. React Oxyg Species (Apex). 2016;1(1):9-21.
41. Kalyanaraman B. Teaching the basics of redox biology to medical and graduate students: Oxidants, antioxidants and disease mechanisms. Redox Biol. 2013;1(1):244-57.
42. Cecchini B., Lourenço-Cecchini A. SARS-CoV-2 infection pathogenesis is related to oxidative stress as a response to aggression. Med Hypotheses. 2020;143:110102.
43. Saleh J., Peyssonnaux C.,, Singh KK., Edeas M. Mito- chondria and microbiota dysfunction in the pathogenesis of COVID-19. Mitochondrion. 2020;54:1-7.
44. Peterhans E. Oxidants and antioxidants in viral diseases: disease mechanisms and metabolic regulation. J Nutr. 1997;127(5 Suppl):962S-965S.
45. Schwartz KB. Oxidative stress during viral infection: a review. .Free Radic Biol Med. 1996;21(5):641-9.46
46. Suresh DR, Annam V, Pratibha K, Prasad BV. Total antioxidant capacity--a novel early bio-chemical marker of oxidative stress in HIV infected individuals. J Biomed Sci. 2009;16(1):61.
47. Delgado-Roche L., Mesta F.. Oxidative stress as a key player in severe acute respiratory syndrome coronavirus (SARS-CoV) infection. Arch Med Res. 2020;51(5):384-387.
48. Firas R.,. Mazhar, A., Ghena K.,; Dunia, S. Amjad A. SARS-CoV2 and Coronavirus Disease 2019: What we know so far. Pathogens. 2020;9(3):231.
49. Edeas M, Saleh J, Peyssonnaux C. Iron: innocent or vi- cious bystander guilty of COVID-19 pathogenesis? Int J Infect Dis. 2020;97:303-305..
50. Laforge M., Elbim C., Frère C., Hémadi M., Massaad C et al. Tissue damage from neutrophil-induced oxidative stress in COVID-19. Nat RevImmunol.2020;20(9):515 –516.
51. Schönrich G, Raftery MJ, Samstag Y. Devilishly radical network in COVID-19: oxidative stress, extracellular neutrophil traps (NET), and T-cell suppression. Adv Biol Regul. 2020;77:100741.52
52. Leppkes M., Knopf J., Naschberger E, Lindemann A., Singh J., Herrmann I. et al. Vascular occlusion by extracellular neutrophil traps in COVID-19. EBioMedicine. 2020; 58:102925.
53. Panfoli I. Potential role of ectopic redox complexes on the surface of endothelial cells in the pathogenesis of COVID-19 disease. Clin Med. 2020;20(5):e146-e147.
54. Lin J.H., Walter P., Yen T.S.B. Endoplasmic reticulum stress in disease pathogenesis. Ann. Rev. Pathol. 2008;3:399–425.
55. Banerjee A, Czinn SJ., Reiter RJ., Blanchard TG. Cross- talk between endoplasmic reticulum stress and anti-viral activities: A novel therapeutic target for COVID-19. Life Sci.2020:255:117842.
56. Li Z., Xu X., Leng X., He M., Wang J., Cheng S et al. Roles of reactive oxygen species in cell signaling path- ways and immune responses to viral infections . Arch Virol.2017;162(3):603-610. 57
57. Ye Q, Wang B, Mao J. The pathogenesis and treatment of the ‘Cytokine Storm’ in COVID-19. J Infect. 2020;80(6):607–613.
58. Foley J.H., Conway E.M. Cross talk pathways between coagulation and inflammation. Circ Res. 2016;118(9):1392–408.
59. Tang N., Li D., Wang X., Sun Z. Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia. J Thromb Haemost. 2020;18:844–847.
60. Zhou F, Yu T, Du R, Fan G, Liu Y, Liu Z et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet. 2020;395(10229):1054-1062.
61. Barzola CM, Parra-Amay CL, Carranza-Delgado KA, Mayorga-Fierro LM. Trastornos de la coagulación en pacientes infectados con coronavirus: Covid-19. RECI- MAUC. 2020;4(3):50-57.
62. José RJ, Williams AE, Chambers RC. Proteinase-activated receptors in fibroproliferative lung disease. Tórax. 2014;69(2):190-192.
63. Fenghe Du, Bao Liu, Shuyang Zhang. COVID-19: the role of excessive cytokine release and possible decrease in ACE2 in promoting the hypercoagulable state associated with severe disease. J Thrombolysis. 202051(2): 1-17.
64. Fehr AR, Channappanavar R , Perlman S. Middle East Respiratory Syndrome: Emergence of a Pathogenic Human Coronavirus. Annu Rev Med.2017;68:387-399.
65. Xiong Y., Liu Y, Cao L., Wang D., Guo M., Jiang A. et al. Transcriptomic characteristics of bronchoalveolar lavage fluid and peripheral blood mononuclear cells in COVID-19 patients. Emerg Microbes Infect. 2020;9(1):761-770.
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Cómo citar
[1]
Camargo Rubio, R.D. 2021. ¿Las especies reactivas del oxígeno y el sistema de defensa antioxidante se relacionan con la respuesta inflamatoria del SARS-CoV-2?. Medicina. 43, 3 (oct. 2021), 382–400. DOI:https://doi.org/10.56050/01205498.1622.
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2021-10-23
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