Oxidative Stress and Its Association with COVID-19: A Narrative Review
https://doi.org/10.24017/covid.11
Abstract views: 4028 / PDF downloads: 1393Abstract
The naturalness of severe acute respiratory syndrome coronavirus 2 infections (SARS-Cov-2) appears to impact the respiratory system and lungs, however, the etiology of many cases exhibited several various features of the disease. The Coronavirus disease 2019 (COVID-19) symptoms are not limited to the virus’s first definitions. This review gathered the contemporary information throughout PubMed, Scopus, and Science Direct databases regarding possible effects of the virus in generating reactive oxygen species and causing oxidative stress. However, this ensures a hypothesis for now, yet from the literature and incidence of COVID-19 symptoms along with comorbidities we can observe the potentials of the virus in the generation of oxidative stress. Especially the virus’s route to cell entry via angiotensin-converting enzyme 2 (ACE2) receptor is well known that leads to pathogenesis in angiotensin II (AT II) which are critical in NADH/NADPH oxidase inducing ROS generation. Moreover, the virus’s activity to replicate seems to be reduced in high antioxidant glutathione level concentrations. The outcome of the review proposes a hypothesis that COVID-19 is associated with reactive oxygen species and its comorbidities mostly joined with oxidative stress including hypertension, cardiovascular, thrombosis, obesity, and diabetes besides of chronic obstructive pulmonary disease and asthma.
Keywords:
ACE2, COVID-19, Oxidative stress, ROS, SARS-CoV-2
References
[1] M. Cascella, M. Rajnik, A. Cuomo, S. C. Dulebohn, and R. Di Napoli, Features, Evaluation and Treatment Coronavirus (COVID-19). StatPearls Publishing, 2020.
[2] C. Huang et al., "Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China.," Lancet (London, England), vol. 395, no. 10223, pp. 497-506, Feb. 2020, doi: 10.1016/S0140-6736(20)30183-5.
https://doi.org/10.1016/S0140-6736(20)30183-5
[3] M. T. Ul Qamar, S. M. Alqahtani, M. A. Alamri, and L.-L. Chen, "Structural basis of SARS-CoV-2 3CL(pro) and anti-COVID-19 drug discovery from medicinal plants.," J. Pharm. Anal., Mar. 2020, doi: 10.1016/j.jpha.2020.03.009.
https://doi.org/10.1016/j.jpha.2020.03.009
[4] Y.-R. Guo et al., "The origin, transmission and clinical therapies on coronavirus disease 2019 (COVID-19) outbreak - an update on the status.," Mil. Med. Res., vol. 7, no. 1, p. 11, Mar. 2020, doi: 10.1186/s40779-020-00240-0.
https://doi.org/10.1186/s40779-020-00240-0
[5] M. Shereen, S. Khan, A. Kazmi, N. Bashir, and R. Siddique, "COVID-19 infection: Origin, transmission, and characteristics of human coronaviruses," J. Adv. Res., vol. 24, Mar. 2020, doi: 10.1016/j.jare.2020.03.005.
https://doi.org/10.1016/j.jare.2020.03.005
[6] P. Zhou et al., "A pneumonia outbreak associated with a new coronavirus of probable bat origin.," Nature, vol. 579, no. 7798, pp. 270-273, Mar. 2020, doi: 10.1038/s41586-020-2012-7.
https://doi.org/10.1038/s41586-020-2012-7
[7] W. Sungnak et al., "SARS-CoV-2 entry factors are highly expressed in nasal epithelial cells together with innate immune genes," Nat. Med., vol. 26, no. May, 2020, doi: 10.1038/s41591-020-0868-6.
https://doi.org/10.1038/s41591-020-0868-6
[8] A. B. Patel and A. Verma, "COVID-19 and Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Blockers: What Is the Evidence?," JAMA, Mar. 2020, doi: 10.1001/jama.2020.4812.
https://doi.org/10.1001/jama.2020.4812
[9] H. Sies, "Oxidative stress: from basic research to clinical application.," Am. J. Med., vol. 91, no. 3C, pp. 31S-38S, Sep. 1991, doi: 10.1016/0002-9343(91)90281-2.
https://doi.org/10.1016/0002-9343(91)90281-2
[10] V. I. Lushchak, "Free radicals, reactive oxygen species, oxidative stress and its classification.," Chem. Biol. Interact., vol. 224, pp. 164-175, Dec. 2014, doi: 10.1016/j.cbi.2014.10.016.
https://doi.org/10.1016/j.cbi.2014.10.016
[11] H. Sies, C. Berndt, and D. P. Jones, "Oxidative Stress.," Annu. Rev. Biochem., vol. 86, pp. 715-748, Jun. 2017, doi: 10.1146/annurev-biochem-061516-045037.
https://doi.org/10.1146/annurev-biochem-061516-045037
[12] D. P. Jones, "Redefining Oxidative Stress," Antioxid. Redox Signal., vol. 8, no. 9-10, pp. 1865-1879, Sep. 2006, doi: 10.1089/ars.2006.8.1865.
https://doi.org/10.1089/ars.2006.8.1865
[13] D. P. Jones, "Radical-free biology of oxidative stress," Am. J. Physiol. Cell Physiol., vol. 295, no. 4, pp. C849-C868, Oct. 2008, doi: 10.1152/ajpcell.00283.2008.
https://doi.org/10.1152/ajpcell.00283.2008
[14] C. P. Stanley et al., "Singlet molecular oxygen regulates vascular tone and blood pressure in inflammation.," Nature, vol. 566, no. 7745, pp. 548-552, Feb. 2019, doi: 10.1038/s41586-019-0947-3.
https://doi.org/10.1038/s41586-019-0947-3
[15] O. A. Khomich, S. N. Kochetkov, B. Bartosch, and A. V Ivanov, "Redox Biology of Respiratory Viral Infections.," Viruses, vol. 10, no. 8, Jul. 2018, doi: 10.3390/v10080392.
https://doi.org/10.3390/v10080392
[16] H. Sies, "Oxidative stress: A concept in redox biology and medicine," Redox Biol., vol. 4, pp. 180-183, 2015, doi: 10.1016/j.redox.2015.01.002.
https://doi.org/10.1016/j.redox.2015.01.002
[17] S. P. Baba and A. Bhatnagar, "ROLE OF THIOLS IN OXIDATIVE STRESS.," Curr. Opin. Toxicol., vol. 7, pp. 133-139, Feb. 2018, doi: 10.1016/j.cotox.2018.03.005.
https://doi.org/10.1016/j.cotox.2018.03.005
[18] C. L. Hawkins and M. J. Davies, "Detection, identification, and quantification of oxidative protein modifications," J. Biol. Chem., vol. 294, no. 51, pp. 19683-19708, Dec. 2019, doi: 10.1074/jbc.REV119.006217.
https://doi.org/10.1074/jbc.REV119.006217
[19] K. K. Griendling et al., "Measurement of Reactive Oxygen Species, Reactive Nitrogen Species, and Redox-Dependent Signaling in the Cardiovascular System: A Scientific Statement From the American Heart Association.," Circ. Res., vol. 119, no. 5, pp. e39-75, Aug. 2016, doi: 10.1161/RES.0000000000000110.
https://doi.org/10.1161/RES.0000000000000110
[20] J. J. Skoko, S. Attaran, and C. A. Neumann, "Signals Getting Crossed in the Entanglement of Redox and Phosphorylation Pathways: Phosphorylation of Peroxiredoxin Proteins Sparks Cell Signaling.," Antioxidants (Basel, Switzerland), vol. 8, no. 2, Jan. 2019, doi: 10.3390/antiox8020029.
https://doi.org/10.3390/antiox8020029
[21] A. Casola, "Respiratory Viral Infections and Subversion of Cellular Antioxidant Defenses," J. Pharmacogenomics Pharmacoproteomics, vol. 05, no. 04, 2014, doi: 10.4172/2153-0645.1000141.
https://doi.org/10.4172/2153-0645.1000141
[22] Y. Higashi, K. Noma, M. Yoshizumi, and Y. Kihara, "Endothelial function and oxidative stress in cardiovascular diseases.," Circ. J., vol. 73, no. 3, pp. 411-418, Mar. 2009, doi: 10.1253/circj.cj-08-1102.
https://doi.org/10.1253/circj.CJ-08-1102
[23] F. Wu et al., "A new coronavirus associated with human respiratory disease in China.," Nature, vol. 579, no. 7798, pp. 265-269, Mar. 2020, doi: 10.1038/s41586-020-2008-3.
https://doi.org/10.1038/s41586-020-2008-3
[24] S. Jiang, C. Hillyer, and L. Du, "Neutralizing Antibodies against SARS-CoV-2 and Other Human Coronaviruses.," Trends Immunol., vol. 41, no. 5, pp. 355-359, May 2020, doi: 10.1016/j.it.2020.03.007.
https://doi.org/10.1016/j.it.2020.03.007
[25] A. R. Fehr and S. Perlman, "Coronaviruses: an overview of their replication and pathogenesis.," Methods Mol. Biol., vol. 1282, pp. 1-23, 2015, doi: 10.1007/978-1-4939-2438-7_1.
https://doi.org/10.1007/978-1-4939-2438-7_1
[26] A. C. Walls, Y.-J. Park, M. A. Tortorici, A. Wall, A. T. McGuire, and D. Veesler, "Structure, Function, and Antigenicity of the SARS-CoV-2 Spike Glycoprotein.," Cell, vol. 181, no. 2, pp. 281-292.e6, Apr. 2020, doi: 10.1016/j.cell.2020.02.058.
https://doi.org/10.1016/j.cell.2020.02.058
[27] H. Xu et al., "High expression of ACE2 receptor of 2019-nCoV on the epithelial cells of oral mucosa," Int. J. Oral Sci., vol. 12, no. 1, p. 8, 2020, doi: 10.1038/s41368-020-0074-x.
https://doi.org/10.1038/s41368-020-0074-x
[28] L. Delgado-Roche and F. Mesta, "Oxidative Stress as Key Player in Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) infection," Arch. Med. Res., no. January, 2020, doi: https://doi.org/10.1016/j.arcmed.2020.04.019. This.
https://doi.org/10.1016/j.arcmed.2020.04.019
[29] G. A. Knock, "NADPH oxidase in the vasculature: Expression, regulation and signalling pathways; role in normal cardiovascular physiology and its dysregulation in hypertension.," Free Radic. Biol. Med., vol. 145, pp. 385-427, Dec. 2019, doi: 10.1016/j.freeradbiomed.2019.09.029.
https://doi.org/10.1016/j.freeradbiomed.2019.09.029
[30] V. J. Dzau, "Theodore Cooper Lecture: Tissue angiotensin and pathobiology of vascular disease: a unifying hypothesis.," Hypertension (Dallas, Tex.?: 1979), vol. 37, no. 4. United States, pp. 1047-1052, Apr. 2001, doi: 10.1161/01.hyp.37.4.1047.
https://doi.org/10.1161/01.HYP.37.4.1047
[31] G. Zalba et al., "Vascular NADH/NADPH oxidase is involved in enhanced superoxide production in spontaneously hypertensive rats.," Hypertens. (Dallas, Tex. 1979), vol. 35, no. 5, pp. 1055-1061, May 2000, doi: 10.1161/01.hyp.35.5.1055.
https://doi.org/10.1161/01.HYP.35.5.1055
[32] R. M. Touyz, "Reactive oxygen species, vascular oxidative stress, and redox signaling in hypertension: what is the clinical significance?," Hypertens. (Dallas, Tex. 1979), vol. 44, no. 3, pp. 248-252, Sep. 2004, doi: 10.1161/01.HYP.0000138070.47616.9d.
https://doi.org/10.1161/01.HYP.0000138070.47616.9d
[33] A. B. Patel and A. Verma, "COVID-19 and Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Blockers: What Is the Evidence?," JAMA - J. Am. Med. Assoc., 2020, doi: 10.1001/jama.2020.4812.
https://doi.org/10.1001/jama.2020.4812
[34] Y. Rautureau and E. L. Schiffrin, "Endothelin in hypertension: an update.," Curr. Opin. Nephrol. Hypertens., vol. 21, no. 2, pp. 128-136, Mar. 2012, doi: 10.1097/MNH.0b013e32834f0092.
https://doi.org/10.1097/MNH.0b013e32834f0092
[35] R. M. Touyz et al., "Vascular smooth muscle contraction in hypertension.," Cardiovasc. Res., vol. 114, no. 4, pp. 529-539, Mar. 2018, doi: 10.1093/cvr/cvy023.
https://doi.org/10.1093/cvr/cvy023
[36] R. Alves-Lopes et al., "Crosstalk Between Vascular Redox and Calcium Signaling in Hypertension Involves TRPM2 (Transient Receptor Potential Melastatin 2) Cation Channel.," Hypertens. (Dallas, Tex. 1979), vol. 75, no. 1, pp. 139-149, Jan. 2020, doi: 10.1161/HYPERTENSIONAHA.119.13861.
https://doi.org/10.1161/HYPERTENSIONAHA.119.13861
[37] J. M. A. Van Den Brand, B. L. Haagmans, D. Van Riel, A. D. M. E. Osterhaus, and T. Kuiken, "ScienceDirect The Pathology and Pathogenesis of Experimental Severe Acute Respiratory Syndrome and Influenza in Animal Models *," J. Comp. Pathol., 2014, doi: 10.1016/j.jcpa.2014.01.004.
https://doi.org/10.1016/j.jcpa.2014.01.004
[38] J. T. Smith, N. J. Willey, and J. T. Hancock, "Low dose ionizing radiation produces too few reactive oxygen species to directly affect antioxidant concentrations in cells," Biol. Lett., vol. 8, no. 4, pp. 594-597, Aug. 2012, doi: 10.1098/rsbl.2012.0150.
https://doi.org/10.1098/rsbl.2012.0150
[39] C.-W. Lin, K.-H. Lin, T.-H. Hsieh, S.-Y. Shiu, and J.-Y. Li, "Severe acute respiratory syndrome coronavirus 3C-like protease-induced apoptosis.," FEMS Immunol. Med. Microbiol., vol. 46, no. 3, pp. 375-380, Apr. 2006, doi: 10.1111/j.1574-695X.2006.00045.x.
https://doi.org/10.1111/j.1574-695X.2006.00045.x
[40] K. Padhan, R. Minakshi, A. Towheed, and S. Jameel, "Severe acute respiratory syndrome coronavirus 3a protein activates the mitochondrial death pathway through p38 MAP kinase activation," J. Gen. Virol., vol. 89, pp. 1960-1969, Aug. 2008, doi: 10.1099/vir.0.83665-0.
https://doi.org/10.1099/vir.0.83665-0
[41] Y. Imai et al., "Identification of oxidative stress and Toll-like receptor 4 signaling as a key pathway of acute lung injury.," Cell, vol. 133, no. 2, pp. 235-249, Apr. 2008, doi: 10.1016/j.cell.2008.02.043.
https://doi.org/10.1016/j.cell.2008.02.043
[42] H. Shao et al., "Upregulation of mitochondrial gene expression in PBMC from convalescent SARS patients," J. Clin. Immunol., vol. 26, no. 6, pp. 546-554, Nov. 2006, doi: 10.1007/s10875-006-9046-y.
https://doi.org/10.1007/s10875-006-9046-y
[43] L. Gil del Valle, R. Gravier Hernández, L. Delgado Roche, and O. S. León Fernández, "Oxidative Stress in the Aging Process: Fundamental Aspects and New Insights," in Oxidative Stress: Diagnostics, Prevention, and Therapy Volume 2, vol. 1200, American Chemical Society, 2015, pp. 177-219 SE-6.
https://doi.org/10.1021/bk-2015-1200.ch006
[44] K. J. A. Davies, "The Oxygen Paradox , oxidative stress , and ageing," Arch. Biochem. Biophys., vol. 595, pp. 28-32, 2016, doi: 10.1016/j.abb.2015.11.015.
https://doi.org/10.1016/j.abb.2015.11.015
[45] S. L. Smits et al., "Exacerbated Innate Host Response to SARS-CoV in Aged Non-Human Primates," vol. 6, no. 2, 2010, doi: 10.1371/journal.ppat.1000756.
https://doi.org/10.1371/journal.ppat.1000756
[46] P. Wenzel, S. Kossmann, T. Munzel, and A. Daiber, "Redox regulation of cardiovascular inflammation - Immunomodulatory function of mitochondrial and Nox-derived reactive oxygen and nitrogen species.," Free Radic. Biol. Med., vol. 109, pp. 48-60, Aug. 2017, doi: 10.1016/j.freeradbiomed.2017.01.027.
https://doi.org/10.1016/j.freeradbiomed.2017.01.027
[47] K. Y. Hood, A. C. Montezano, A. P. Harvey, M. Nilsen, M. R. MacLean, and R. M. Touyz, "Nicotinamide Adenine Dinucleotide Phosphate Oxidase-Mediated Redox Signaling and Vascular Remodeling by 16alpha-Hydroxyestrone in Human Pulmonary Artery Cells: Implications in Pulmonary Arterial Hypertension.," Hypertens. (Dallas, Tex. 1979), vol. 68, no. 3, pp. 796-808, Sep. 2016, doi: 10.1161/HYPERTENSIONAHA.116.07668.
https://doi.org/10.1161/HYPERTENSIONAHA.116.07668
[48] S. Vukelic and K. K. Griendling, "Angiotensin II, from vasoconstrictor to growth factor: a paradigm shift.," Circ. Res., vol. 114, no. 5, pp. 754-757, Feb. 2014, doi: 10.1161/CIRCRESAHA.114.303045.
https://doi.org/10.1161/CIRCRESAHA.114.303045
[49] P. D. Ray, B.-W. Huang, and Y. Tsuji, "Reactive oxygen species (ROS) homeostasis and redox regulation in cellular signaling.," Cell. Signal., vol. 24, no. 5, pp. 981-990, May 2012, doi: 10.1016/j.cellsig.2012.01.008.
https://doi.org/10.1016/j.cellsig.2012.01.008
[50] A. B. Garcia-Redondo et al., "c-Src, ERK1/2 and Rho kinase mediate hydrogen peroxide-induced vascular contraction in hypertension: role of TXA2, NAD(P)H oxidase and mitochondria.," J. Hypertens., vol. 33, no. 1, pp. 77-87, Jan. 2015, doi: 10.1097/HJH.0000000000000383.
https://doi.org/10.1097/HJH.0000000000000383
[51] Z. Wei, R. M. Salmon, P. D. Upton, N. W. Morrell, and W. Li, "Regulation of bone morphogenetic protein 9 (BMP9) by redox-dependent proteolysis.," J. Biol. Chem., vol. 289, no. 45, pp. 31150-31159, Nov. 2014, doi: 10.1074/jbc.M114.579771.
https://doi.org/10.1074/jbc.M114.579771
[52] Y.-M. Kim, S.-J. Kim, R. Tatsunami, H. Yamamura, T. Fukai, and M. Ushio-Fukai, "ROS-induced ROS release orchestrated by Nox4, Nox2, and mitochondria in VEGF signaling and angiogenesis.," Am. J. Physiol. Cell Physiol., vol. 312, no. 6, pp. C749-C764, Jun. 2017, doi: 10.1152/ajpcell.00346.2016.
https://doi.org/10.1152/ajpcell.00346.2016
[53] R. JF, R. DG, and Y. C. LL., "Sex, oxidative stress, and hypertension: Insights from animal models.," Physiol., vol. 34, pp. 178-88, 2019.
https://doi.org/10.1152/physiol.00035.2018
[54] T. Ide et al., "Greater oxidative stress in healthy young men compared with premenopausal women.," Arterioscler. Thromb. Vasc. Biol., vol. 22, no. 3, pp. 438-442, Mar. 2002, doi: 10.1161/hq0302.104515.
https://doi.org/10.1161/hq0302.104515
[55] K. Bhatia, A. A. Elmarakby, A. B. El-Remessy, and J. C. Sullivan, "Oxidative stress contributes to sex differences in angiotensin II-mediated hypertension in spontaneously hypertensive rats.," Am. J. Physiol. Regul. Integr. Comp. Physiol., vol. 302, no. 2, pp. R274-82, Jan. 2012, doi: 10.1152/ajpregu.00546.2011.
https://doi.org/10.1152/ajpregu.00546.2011
[56] H. Sies, "Oxidative stress: impact in redox biology and medicine," Arch. Med. Biomed. Res., vol. 2, no. 4, p. 146, 2016, doi: 10.4314/ambr.v2i4.6.
https://doi.org/10.4314/ambr.v2i4.6
[57] H. Sies, "Hydrogen peroxide as a central redox signaling molecule in physiological oxidative stress: Oxidative eustress.," Redox Biol., vol. 11, pp. 613-619, Apr. 2017, doi: 10.1016/j.redox.2016.12.035.
https://doi.org/10.1016/j.redox.2016.12.035
[58] A. Ore and O. A. Akinloye, "Oxidative Stress and Antioxidant Biomarkers in Clinical and Experimental Models of Non-Alcoholic Fatty Liver Disease," Medicina (Kaunas)., vol. 55, no. 2, p. 26, Jan. 2019, doi: 10.3390/medicina55020026.
https://doi.org/10.3390/medicina55020026
[59] R. F. Furchgott and J. V Zawadzki, "The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine.," Nature, vol. 288, no. 5789, pp. 373-376, Nov. 1980, doi: 10.1038/288373a0.
https://doi.org/10.1038/288373a0
[60] L. J. Ignarro, R. E. Byrns, G. M. Buga, K. S. Wood, and G. Chaudhuri, "Pharmacological evidence that endothelium-derived relaxing factor is nitric oxide: use of pyrogallol and superoxide dismutase to study endothelium-dependent and nitric oxide-elicited vascular smooth muscle relaxation.," J. Pharmacol. Exp. Ther., vol. 244, no. 1, pp. 181-189, Jan. 1988.
[61] G. Ferrer-Sueta et al., "Biochemistry of Peroxynitrite and Protein Tyrosine Nitration.," Chem. Rev., vol. 118, no. 3, pp. 1338-1408, Feb. 2018, doi: 10.1021/acs.chemrev.7b00568.
https://doi.org/10.1021/acs.chemrev.7b00568
[62] M. A. Incalza, R. D'Oria, A. Natalicchio, S. Perrini, L. Laviola, and F. Giorgino, "Oxidative stress and reactive oxygen species in endothelial dysfunction associated with cardiovascular and metabolic diseases.," Vascul. Pharmacol., vol. 100, pp. 1-19, Jan. 2018, doi: 10.1016/j.vph.2017.05.005.
https://doi.org/10.1016/j.vph.2017.05.005
[63] F. M. Faraci and S. P. Didion, "Vascular protection: superoxide dismutase isoforms in the vessel wall.," Arterioscler. Thromb. Vasc. Biol., vol. 24, no. 8, pp. 1367-1373, Aug. 2004, doi: 10.1161/01.ATV.0000133604.20182.cf.
https://doi.org/10.1161/01.ATV.0000133604.20182.cf
[64] H. J. Forman, H. Zhang, and A. Rinna, "Glutathione: overview of its protective roles, measurement, and biosynthesis.," Mol. Aspects Med., vol. 30, no. 1-2, pp. 1-12, 2009, doi: 10.1016/j.mam.2008.08.006.
https://doi.org/10.1016/j.mam.2008.08.006
[65] J. Pizzorno, "Glutathione!," Integr. Med. (Encinitas)., vol. 13, no. 1, pp. 8-12, Feb. 2014, [Online]. Available: https://pubmed.ncbi.nlm.nih.gov/26770075.
[66] A. Polonikov, Endogenous deficiency of glutathione as the most likely cause of serious manifestations and death in patients with the novel coronavirus infection (COVID-19): a hypothesis based on literature data and own observations. 2020.
https://doi.org/10.1021/acsinfecdis.0c00288
[67] Z. Varga et al., "Endothelial cell infection and endotheliitis in COVID-19," Lancet, vol. 395, no. 10234, pp. 1417-1418, 2020, doi: 10.1016/S0140-6736(20)30937-5.
https://doi.org/10.1016/S0140-6736(20)30937-5
[68] F. A. Klok et al., "Incidence of thrombotic complications in critically ill ICU patients with COVID-19," Thromb. Res., no. xxxx, pp. 1-3, 2020, doi: 10.1016/j.thromres.2020.04.013.
https://doi.org/10.1016/j.thromres.2020.04.013
[69] N. R. Madamanchi, Z. S. Hakim, and M. S. Runge, "Oxidative stress in atherogenesis and arterial thrombosis: The disconnect between cellular studies and clinical outcomes," J. Thromb. Haemost., vol. 3, no. 2, pp. 254-267, 2005, doi: 10.1111/j.1538-7836.2004.01085.x.
https://doi.org/10.1111/j.1538-7836.2004.01085.x
[70] N. R. Brady, A. Hamacher-Brady, H. V Westerhoff, and R. A. Gottlieb, "A wave of reactive oxygen species (ROS)-induced ROS release in a sea of excitable mitochondria.," Antioxid. Redox Signal., vol. 8, no. 9-10, pp. 1651-1665, 2006, doi: 10.1089/ars.2006.8.1651.
https://doi.org/10.1089/ars.2006.8.1651
[71] D. B. Zorov, M. Juhaszova, and S. J. Sollott, "Mitochondrial ROS-induced ROS release: an update and review.," Biochim. Biophys. Acta, vol. 1757, no. 5-6, pp. 509-517, 2006, doi: 10.1016/j.bbabio.2006.04.029.
https://doi.org/10.1016/j.bbabio.2006.04.029
[72] E. Prompetchara, C. Ketloy, and T. Palaga, "Immune responses in COVID-19 and potential vaccines: Lessons learned from SARS and MERS epidemic," Asian Pacific J. allergy Immunol., vol. 38, no. 1, pp. 1-9, 2020, doi: 10.12932/AP-200220-0772.
https://doi.org/10.12932/AP-200220-0772
[73] G. T. Nguyen, E. R. Green, and J. Mecsas, "Neutrophils to the ROScue: Mechanisms of NADPH Oxidase Activation and Bacterial Resistance," Front. Cell. Infect. Microbiol., vol. 7, p. 373, Aug. 2017, doi: 10.3389/fcimb.2017.00373.
https://doi.org/10.3389/fcimb.2017.00373
[74] F. Lovren et al., "Angiotensin converting enzyme-2 confers endothelial protection and attenuates atherosclerosis.," Am. J. Physiol. Heart Circ. Physiol., vol. 295, no. 4, pp. H1377-84, Oct. 2008, doi: 10.1152/ajpheart.00331.2008.
https://doi.org/10.1152/ajpheart.00331.2008
[75] Y.-H. Zhang et al., "ACE2 and Ang-(1-7) protect endothelial cell function and prevent early atherosclerosis by inhibiting inflammatory response.," Inflamm. Res., vol. 64, no. 3-4, pp. 253-260, Apr. 2015, doi: 10.1007/s00011-015-0805-1.
https://doi.org/10.1007/s00011-015-0805-1
[76] et al., "Presenting Characteristics, Comorbidities, and Outcomes Among 5700 Patients Hospitalized With COVID-19 in the New York City Area," Jama, vol. 10022, pp. 1-8, 2020, doi: 10.1001/jama.2020.6775.
https://doi.org/10.1001/jama.2020.6775
[77] M. Nozoe et al., "Mitochondria-derived reactive oxygen species mediate sympathoexcitation induced by angiotensin II in the rostral ventrolateral medulla," J. Hypertens., vol. 26, no. 11, p. 2176-2184, Nov. 2008, doi: 10.1097/hjh.0b013e32830dd5d3.
https://doi.org/10.1097/HJH.0b013e32830dd5d3
[78] S. I. Dikalov and Z. Ungvari, "Role of mitochondrial oxidative stress in hypertension.," Am. J. Physiol. Heart Circ. Physiol., vol. 305, no. 10, pp. H1417-27, Nov. 2013, doi: 10.1152/ajpheart.00089.2013.
https://doi.org/10.1152/ajpheart.00089.2013
[79] V. R. Vaka et al., "Blockade of endogenous angiotensin II type I receptor agonistic autoantibody activity improves mitochondrial reactive oxygen species and hypertension in a rat model of preeclampsia.," Am. J. Physiol. Regul. Integr. Comp. Physiol., vol. 318, no. 2, pp. R256-R262, Feb. 2020, doi: 10.1152/ajpregu.00179.2019.
https://doi.org/10.1152/ajpregu.00179.2019
[80] J. Gonzalez, N. Valls, R. Brito, and R. Rodrigo, "Essential hypertension and oxidative stress: New insights.," World J. Cardiol., vol. 6, no. 6, pp. 353-366, Jun. 2014, doi: 10.4330/wjc.v6.i6.353.
https://doi.org/10.4330/wjc.v6.i6.353
[81] R. M. Touyz, G. Yao, M. T. Quinn, P. J. Pagano, and E. L. Schiffrin, "p47phox associates with the cytoskeleton through cortactin in human vascular smooth muscle cells: role in NAD(P)H oxidase regulation by angiotensin II.," Arterioscler. Thromb. Vasc. Biol., vol. 25, no. 3, pp. 512-518, Mar. 2005, doi: 10.1161/01.ATV.0000154141.66879.98.
https://doi.org/10.1161/01.ATV.0000154141.66879.98
[82] C. N. Young, "Endoplasmic reticulum stress in the pathogenesis of hypertension.," Exp. Physiol., vol. 102, no. 8, pp. 869-884, Aug. 2017, doi: 10.1113/EP086274.
https://doi.org/10.1113/EP086274
[83] C. X. C. Santos, A. A. Nabeebaccus, A. M. Shah, L. L. Camargo, S. V Filho, and L. R. Lopes, "Endoplasmic reticulum stress and Nox-mediated reactive oxygen species signaling in the peripheral vasculature: potential role in hypertension.," Antioxid. Redox Signal., vol. 20, no. 1, pp. 121-134, Jan. 2014, doi: 10.1089/ars.2013.5262.
https://doi.org/10.1089/ars.2013.5262
[84] A. S. Fauci, H. C. Lane, and R. R. Redfield, "Covid-19 - Navigating the Uncharted.," The New England journal of medicine, vol. 382, no. 13. United States, pp. 1268-1269, Mar. 2020, doi: 10.1056/NEJMe2002387.
https://doi.org/10.1056/NEJMe2002387
[85] R. E. Jordan, P. Adab, and K. K. Cheng, "Covid-19: risk factors for severe disease and death," BMJ, vol. 368, p. m1198, Mar. 2020, doi: 10.1136/bmj.m1198.
https://doi.org/10.1136/bmj.m1198
[2] C. Huang et al., "Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China.," Lancet (London, England), vol. 395, no. 10223, pp. 497-506, Feb. 2020, doi: 10.1016/S0140-6736(20)30183-5.
https://doi.org/10.1016/S0140-6736(20)30183-5
[3] M. T. Ul Qamar, S. M. Alqahtani, M. A. Alamri, and L.-L. Chen, "Structural basis of SARS-CoV-2 3CL(pro) and anti-COVID-19 drug discovery from medicinal plants.," J. Pharm. Anal., Mar. 2020, doi: 10.1016/j.jpha.2020.03.009.
https://doi.org/10.1016/j.jpha.2020.03.009
[4] Y.-R. Guo et al., "The origin, transmission and clinical therapies on coronavirus disease 2019 (COVID-19) outbreak - an update on the status.," Mil. Med. Res., vol. 7, no. 1, p. 11, Mar. 2020, doi: 10.1186/s40779-020-00240-0.
https://doi.org/10.1186/s40779-020-00240-0
[5] M. Shereen, S. Khan, A. Kazmi, N. Bashir, and R. Siddique, "COVID-19 infection: Origin, transmission, and characteristics of human coronaviruses," J. Adv. Res., vol. 24, Mar. 2020, doi: 10.1016/j.jare.2020.03.005.
https://doi.org/10.1016/j.jare.2020.03.005
[6] P. Zhou et al., "A pneumonia outbreak associated with a new coronavirus of probable bat origin.," Nature, vol. 579, no. 7798, pp. 270-273, Mar. 2020, doi: 10.1038/s41586-020-2012-7.
https://doi.org/10.1038/s41586-020-2012-7
[7] W. Sungnak et al., "SARS-CoV-2 entry factors are highly expressed in nasal epithelial cells together with innate immune genes," Nat. Med., vol. 26, no. May, 2020, doi: 10.1038/s41591-020-0868-6.
https://doi.org/10.1038/s41591-020-0868-6
[8] A. B. Patel and A. Verma, "COVID-19 and Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Blockers: What Is the Evidence?," JAMA, Mar. 2020, doi: 10.1001/jama.2020.4812.
https://doi.org/10.1001/jama.2020.4812
[9] H. Sies, "Oxidative stress: from basic research to clinical application.," Am. J. Med., vol. 91, no. 3C, pp. 31S-38S, Sep. 1991, doi: 10.1016/0002-9343(91)90281-2.
https://doi.org/10.1016/0002-9343(91)90281-2
[10] V. I. Lushchak, "Free radicals, reactive oxygen species, oxidative stress and its classification.," Chem. Biol. Interact., vol. 224, pp. 164-175, Dec. 2014, doi: 10.1016/j.cbi.2014.10.016.
https://doi.org/10.1016/j.cbi.2014.10.016
[11] H. Sies, C. Berndt, and D. P. Jones, "Oxidative Stress.," Annu. Rev. Biochem., vol. 86, pp. 715-748, Jun. 2017, doi: 10.1146/annurev-biochem-061516-045037.
https://doi.org/10.1146/annurev-biochem-061516-045037
[12] D. P. Jones, "Redefining Oxidative Stress," Antioxid. Redox Signal., vol. 8, no. 9-10, pp. 1865-1879, Sep. 2006, doi: 10.1089/ars.2006.8.1865.
https://doi.org/10.1089/ars.2006.8.1865
[13] D. P. Jones, "Radical-free biology of oxidative stress," Am. J. Physiol. Cell Physiol., vol. 295, no. 4, pp. C849-C868, Oct. 2008, doi: 10.1152/ajpcell.00283.2008.
https://doi.org/10.1152/ajpcell.00283.2008
[14] C. P. Stanley et al., "Singlet molecular oxygen regulates vascular tone and blood pressure in inflammation.," Nature, vol. 566, no. 7745, pp. 548-552, Feb. 2019, doi: 10.1038/s41586-019-0947-3.
https://doi.org/10.1038/s41586-019-0947-3
[15] O. A. Khomich, S. N. Kochetkov, B. Bartosch, and A. V Ivanov, "Redox Biology of Respiratory Viral Infections.," Viruses, vol. 10, no. 8, Jul. 2018, doi: 10.3390/v10080392.
https://doi.org/10.3390/v10080392
[16] H. Sies, "Oxidative stress: A concept in redox biology and medicine," Redox Biol., vol. 4, pp. 180-183, 2015, doi: 10.1016/j.redox.2015.01.002.
https://doi.org/10.1016/j.redox.2015.01.002
[17] S. P. Baba and A. Bhatnagar, "ROLE OF THIOLS IN OXIDATIVE STRESS.," Curr. Opin. Toxicol., vol. 7, pp. 133-139, Feb. 2018, doi: 10.1016/j.cotox.2018.03.005.
https://doi.org/10.1016/j.cotox.2018.03.005
[18] C. L. Hawkins and M. J. Davies, "Detection, identification, and quantification of oxidative protein modifications," J. Biol. Chem., vol. 294, no. 51, pp. 19683-19708, Dec. 2019, doi: 10.1074/jbc.REV119.006217.
https://doi.org/10.1074/jbc.REV119.006217
[19] K. K. Griendling et al., "Measurement of Reactive Oxygen Species, Reactive Nitrogen Species, and Redox-Dependent Signaling in the Cardiovascular System: A Scientific Statement From the American Heart Association.," Circ. Res., vol. 119, no. 5, pp. e39-75, Aug. 2016, doi: 10.1161/RES.0000000000000110.
https://doi.org/10.1161/RES.0000000000000110
[20] J. J. Skoko, S. Attaran, and C. A. Neumann, "Signals Getting Crossed in the Entanglement of Redox and Phosphorylation Pathways: Phosphorylation of Peroxiredoxin Proteins Sparks Cell Signaling.," Antioxidants (Basel, Switzerland), vol. 8, no. 2, Jan. 2019, doi: 10.3390/antiox8020029.
https://doi.org/10.3390/antiox8020029
[21] A. Casola, "Respiratory Viral Infections and Subversion of Cellular Antioxidant Defenses," J. Pharmacogenomics Pharmacoproteomics, vol. 05, no. 04, 2014, doi: 10.4172/2153-0645.1000141.
https://doi.org/10.4172/2153-0645.1000141
[22] Y. Higashi, K. Noma, M. Yoshizumi, and Y. Kihara, "Endothelial function and oxidative stress in cardiovascular diseases.," Circ. J., vol. 73, no. 3, pp. 411-418, Mar. 2009, doi: 10.1253/circj.cj-08-1102.
https://doi.org/10.1253/circj.CJ-08-1102
[23] F. Wu et al., "A new coronavirus associated with human respiratory disease in China.," Nature, vol. 579, no. 7798, pp. 265-269, Mar. 2020, doi: 10.1038/s41586-020-2008-3.
https://doi.org/10.1038/s41586-020-2008-3
[24] S. Jiang, C. Hillyer, and L. Du, "Neutralizing Antibodies against SARS-CoV-2 and Other Human Coronaviruses.," Trends Immunol., vol. 41, no. 5, pp. 355-359, May 2020, doi: 10.1016/j.it.2020.03.007.
https://doi.org/10.1016/j.it.2020.03.007
[25] A. R. Fehr and S. Perlman, "Coronaviruses: an overview of their replication and pathogenesis.," Methods Mol. Biol., vol. 1282, pp. 1-23, 2015, doi: 10.1007/978-1-4939-2438-7_1.
https://doi.org/10.1007/978-1-4939-2438-7_1
[26] A. C. Walls, Y.-J. Park, M. A. Tortorici, A. Wall, A. T. McGuire, and D. Veesler, "Structure, Function, and Antigenicity of the SARS-CoV-2 Spike Glycoprotein.," Cell, vol. 181, no. 2, pp. 281-292.e6, Apr. 2020, doi: 10.1016/j.cell.2020.02.058.
https://doi.org/10.1016/j.cell.2020.02.058
[27] H. Xu et al., "High expression of ACE2 receptor of 2019-nCoV on the epithelial cells of oral mucosa," Int. J. Oral Sci., vol. 12, no. 1, p. 8, 2020, doi: 10.1038/s41368-020-0074-x.
https://doi.org/10.1038/s41368-020-0074-x
[28] L. Delgado-Roche and F. Mesta, "Oxidative Stress as Key Player in Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) infection," Arch. Med. Res., no. January, 2020, doi: https://doi.org/10.1016/j.arcmed.2020.04.019. This.
https://doi.org/10.1016/j.arcmed.2020.04.019
[29] G. A. Knock, "NADPH oxidase in the vasculature: Expression, regulation and signalling pathways; role in normal cardiovascular physiology and its dysregulation in hypertension.," Free Radic. Biol. Med., vol. 145, pp. 385-427, Dec. 2019, doi: 10.1016/j.freeradbiomed.2019.09.029.
https://doi.org/10.1016/j.freeradbiomed.2019.09.029
[30] V. J. Dzau, "Theodore Cooper Lecture: Tissue angiotensin and pathobiology of vascular disease: a unifying hypothesis.," Hypertension (Dallas, Tex.?: 1979), vol. 37, no. 4. United States, pp. 1047-1052, Apr. 2001, doi: 10.1161/01.hyp.37.4.1047.
https://doi.org/10.1161/01.HYP.37.4.1047
[31] G. Zalba et al., "Vascular NADH/NADPH oxidase is involved in enhanced superoxide production in spontaneously hypertensive rats.," Hypertens. (Dallas, Tex. 1979), vol. 35, no. 5, pp. 1055-1061, May 2000, doi: 10.1161/01.hyp.35.5.1055.
https://doi.org/10.1161/01.HYP.35.5.1055
[32] R. M. Touyz, "Reactive oxygen species, vascular oxidative stress, and redox signaling in hypertension: what is the clinical significance?," Hypertens. (Dallas, Tex. 1979), vol. 44, no. 3, pp. 248-252, Sep. 2004, doi: 10.1161/01.HYP.0000138070.47616.9d.
https://doi.org/10.1161/01.HYP.0000138070.47616.9d
[33] A. B. Patel and A. Verma, "COVID-19 and Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Blockers: What Is the Evidence?," JAMA - J. Am. Med. Assoc., 2020, doi: 10.1001/jama.2020.4812.
https://doi.org/10.1001/jama.2020.4812
[34] Y. Rautureau and E. L. Schiffrin, "Endothelin in hypertension: an update.," Curr. Opin. Nephrol. Hypertens., vol. 21, no. 2, pp. 128-136, Mar. 2012, doi: 10.1097/MNH.0b013e32834f0092.
https://doi.org/10.1097/MNH.0b013e32834f0092
[35] R. M. Touyz et al., "Vascular smooth muscle contraction in hypertension.," Cardiovasc. Res., vol. 114, no. 4, pp. 529-539, Mar. 2018, doi: 10.1093/cvr/cvy023.
https://doi.org/10.1093/cvr/cvy023
[36] R. Alves-Lopes et al., "Crosstalk Between Vascular Redox and Calcium Signaling in Hypertension Involves TRPM2 (Transient Receptor Potential Melastatin 2) Cation Channel.," Hypertens. (Dallas, Tex. 1979), vol. 75, no. 1, pp. 139-149, Jan. 2020, doi: 10.1161/HYPERTENSIONAHA.119.13861.
https://doi.org/10.1161/HYPERTENSIONAHA.119.13861
[37] J. M. A. Van Den Brand, B. L. Haagmans, D. Van Riel, A. D. M. E. Osterhaus, and T. Kuiken, "ScienceDirect The Pathology and Pathogenesis of Experimental Severe Acute Respiratory Syndrome and Influenza in Animal Models *," J. Comp. Pathol., 2014, doi: 10.1016/j.jcpa.2014.01.004.
https://doi.org/10.1016/j.jcpa.2014.01.004
[38] J. T. Smith, N. J. Willey, and J. T. Hancock, "Low dose ionizing radiation produces too few reactive oxygen species to directly affect antioxidant concentrations in cells," Biol. Lett., vol. 8, no. 4, pp. 594-597, Aug. 2012, doi: 10.1098/rsbl.2012.0150.
https://doi.org/10.1098/rsbl.2012.0150
[39] C.-W. Lin, K.-H. Lin, T.-H. Hsieh, S.-Y. Shiu, and J.-Y. Li, "Severe acute respiratory syndrome coronavirus 3C-like protease-induced apoptosis.," FEMS Immunol. Med. Microbiol., vol. 46, no. 3, pp. 375-380, Apr. 2006, doi: 10.1111/j.1574-695X.2006.00045.x.
https://doi.org/10.1111/j.1574-695X.2006.00045.x
[40] K. Padhan, R. Minakshi, A. Towheed, and S. Jameel, "Severe acute respiratory syndrome coronavirus 3a protein activates the mitochondrial death pathway through p38 MAP kinase activation," J. Gen. Virol., vol. 89, pp. 1960-1969, Aug. 2008, doi: 10.1099/vir.0.83665-0.
https://doi.org/10.1099/vir.0.83665-0
[41] Y. Imai et al., "Identification of oxidative stress and Toll-like receptor 4 signaling as a key pathway of acute lung injury.," Cell, vol. 133, no. 2, pp. 235-249, Apr. 2008, doi: 10.1016/j.cell.2008.02.043.
https://doi.org/10.1016/j.cell.2008.02.043
[42] H. Shao et al., "Upregulation of mitochondrial gene expression in PBMC from convalescent SARS patients," J. Clin. Immunol., vol. 26, no. 6, pp. 546-554, Nov. 2006, doi: 10.1007/s10875-006-9046-y.
https://doi.org/10.1007/s10875-006-9046-y
[43] L. Gil del Valle, R. Gravier Hernández, L. Delgado Roche, and O. S. León Fernández, "Oxidative Stress in the Aging Process: Fundamental Aspects and New Insights," in Oxidative Stress: Diagnostics, Prevention, and Therapy Volume 2, vol. 1200, American Chemical Society, 2015, pp. 177-219 SE-6.
https://doi.org/10.1021/bk-2015-1200.ch006
[44] K. J. A. Davies, "The Oxygen Paradox , oxidative stress , and ageing," Arch. Biochem. Biophys., vol. 595, pp. 28-32, 2016, doi: 10.1016/j.abb.2015.11.015.
https://doi.org/10.1016/j.abb.2015.11.015
[45] S. L. Smits et al., "Exacerbated Innate Host Response to SARS-CoV in Aged Non-Human Primates," vol. 6, no. 2, 2010, doi: 10.1371/journal.ppat.1000756.
https://doi.org/10.1371/journal.ppat.1000756
[46] P. Wenzel, S. Kossmann, T. Munzel, and A. Daiber, "Redox regulation of cardiovascular inflammation - Immunomodulatory function of mitochondrial and Nox-derived reactive oxygen and nitrogen species.," Free Radic. Biol. Med., vol. 109, pp. 48-60, Aug. 2017, doi: 10.1016/j.freeradbiomed.2017.01.027.
https://doi.org/10.1016/j.freeradbiomed.2017.01.027
[47] K. Y. Hood, A. C. Montezano, A. P. Harvey, M. Nilsen, M. R. MacLean, and R. M. Touyz, "Nicotinamide Adenine Dinucleotide Phosphate Oxidase-Mediated Redox Signaling and Vascular Remodeling by 16alpha-Hydroxyestrone in Human Pulmonary Artery Cells: Implications in Pulmonary Arterial Hypertension.," Hypertens. (Dallas, Tex. 1979), vol. 68, no. 3, pp. 796-808, Sep. 2016, doi: 10.1161/HYPERTENSIONAHA.116.07668.
https://doi.org/10.1161/HYPERTENSIONAHA.116.07668
[48] S. Vukelic and K. K. Griendling, "Angiotensin II, from vasoconstrictor to growth factor: a paradigm shift.," Circ. Res., vol. 114, no. 5, pp. 754-757, Feb. 2014, doi: 10.1161/CIRCRESAHA.114.303045.
https://doi.org/10.1161/CIRCRESAHA.114.303045
[49] P. D. Ray, B.-W. Huang, and Y. Tsuji, "Reactive oxygen species (ROS) homeostasis and redox regulation in cellular signaling.," Cell. Signal., vol. 24, no. 5, pp. 981-990, May 2012, doi: 10.1016/j.cellsig.2012.01.008.
https://doi.org/10.1016/j.cellsig.2012.01.008
[50] A. B. Garcia-Redondo et al., "c-Src, ERK1/2 and Rho kinase mediate hydrogen peroxide-induced vascular contraction in hypertension: role of TXA2, NAD(P)H oxidase and mitochondria.," J. Hypertens., vol. 33, no. 1, pp. 77-87, Jan. 2015, doi: 10.1097/HJH.0000000000000383.
https://doi.org/10.1097/HJH.0000000000000383
[51] Z. Wei, R. M. Salmon, P. D. Upton, N. W. Morrell, and W. Li, "Regulation of bone morphogenetic protein 9 (BMP9) by redox-dependent proteolysis.," J. Biol. Chem., vol. 289, no. 45, pp. 31150-31159, Nov. 2014, doi: 10.1074/jbc.M114.579771.
https://doi.org/10.1074/jbc.M114.579771
[52] Y.-M. Kim, S.-J. Kim, R. Tatsunami, H. Yamamura, T. Fukai, and M. Ushio-Fukai, "ROS-induced ROS release orchestrated by Nox4, Nox2, and mitochondria in VEGF signaling and angiogenesis.," Am. J. Physiol. Cell Physiol., vol. 312, no. 6, pp. C749-C764, Jun. 2017, doi: 10.1152/ajpcell.00346.2016.
https://doi.org/10.1152/ajpcell.00346.2016
[53] R. JF, R. DG, and Y. C. LL., "Sex, oxidative stress, and hypertension: Insights from animal models.," Physiol., vol. 34, pp. 178-88, 2019.
https://doi.org/10.1152/physiol.00035.2018
[54] T. Ide et al., "Greater oxidative stress in healthy young men compared with premenopausal women.," Arterioscler. Thromb. Vasc. Biol., vol. 22, no. 3, pp. 438-442, Mar. 2002, doi: 10.1161/hq0302.104515.
https://doi.org/10.1161/hq0302.104515
[55] K. Bhatia, A. A. Elmarakby, A. B. El-Remessy, and J. C. Sullivan, "Oxidative stress contributes to sex differences in angiotensin II-mediated hypertension in spontaneously hypertensive rats.," Am. J. Physiol. Regul. Integr. Comp. Physiol., vol. 302, no. 2, pp. R274-82, Jan. 2012, doi: 10.1152/ajpregu.00546.2011.
https://doi.org/10.1152/ajpregu.00546.2011
[56] H. Sies, "Oxidative stress: impact in redox biology and medicine," Arch. Med. Biomed. Res., vol. 2, no. 4, p. 146, 2016, doi: 10.4314/ambr.v2i4.6.
https://doi.org/10.4314/ambr.v2i4.6
[57] H. Sies, "Hydrogen peroxide as a central redox signaling molecule in physiological oxidative stress: Oxidative eustress.," Redox Biol., vol. 11, pp. 613-619, Apr. 2017, doi: 10.1016/j.redox.2016.12.035.
https://doi.org/10.1016/j.redox.2016.12.035
[58] A. Ore and O. A. Akinloye, "Oxidative Stress and Antioxidant Biomarkers in Clinical and Experimental Models of Non-Alcoholic Fatty Liver Disease," Medicina (Kaunas)., vol. 55, no. 2, p. 26, Jan. 2019, doi: 10.3390/medicina55020026.
https://doi.org/10.3390/medicina55020026
[59] R. F. Furchgott and J. V Zawadzki, "The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine.," Nature, vol. 288, no. 5789, pp. 373-376, Nov. 1980, doi: 10.1038/288373a0.
https://doi.org/10.1038/288373a0
[60] L. J. Ignarro, R. E. Byrns, G. M. Buga, K. S. Wood, and G. Chaudhuri, "Pharmacological evidence that endothelium-derived relaxing factor is nitric oxide: use of pyrogallol and superoxide dismutase to study endothelium-dependent and nitric oxide-elicited vascular smooth muscle relaxation.," J. Pharmacol. Exp. Ther., vol. 244, no. 1, pp. 181-189, Jan. 1988.
[61] G. Ferrer-Sueta et al., "Biochemistry of Peroxynitrite and Protein Tyrosine Nitration.," Chem. Rev., vol. 118, no. 3, pp. 1338-1408, Feb. 2018, doi: 10.1021/acs.chemrev.7b00568.
https://doi.org/10.1021/acs.chemrev.7b00568
[62] M. A. Incalza, R. D'Oria, A. Natalicchio, S. Perrini, L. Laviola, and F. Giorgino, "Oxidative stress and reactive oxygen species in endothelial dysfunction associated with cardiovascular and metabolic diseases.," Vascul. Pharmacol., vol. 100, pp. 1-19, Jan. 2018, doi: 10.1016/j.vph.2017.05.005.
https://doi.org/10.1016/j.vph.2017.05.005
[63] F. M. Faraci and S. P. Didion, "Vascular protection: superoxide dismutase isoforms in the vessel wall.," Arterioscler. Thromb. Vasc. Biol., vol. 24, no. 8, pp. 1367-1373, Aug. 2004, doi: 10.1161/01.ATV.0000133604.20182.cf.
https://doi.org/10.1161/01.ATV.0000133604.20182.cf
[64] H. J. Forman, H. Zhang, and A. Rinna, "Glutathione: overview of its protective roles, measurement, and biosynthesis.," Mol. Aspects Med., vol. 30, no. 1-2, pp. 1-12, 2009, doi: 10.1016/j.mam.2008.08.006.
https://doi.org/10.1016/j.mam.2008.08.006
[65] J. Pizzorno, "Glutathione!," Integr. Med. (Encinitas)., vol. 13, no. 1, pp. 8-12, Feb. 2014, [Online]. Available: https://pubmed.ncbi.nlm.nih.gov/26770075.
[66] A. Polonikov, Endogenous deficiency of glutathione as the most likely cause of serious manifestations and death in patients with the novel coronavirus infection (COVID-19): a hypothesis based on literature data and own observations. 2020.
https://doi.org/10.1021/acsinfecdis.0c00288
[67] Z. Varga et al., "Endothelial cell infection and endotheliitis in COVID-19," Lancet, vol. 395, no. 10234, pp. 1417-1418, 2020, doi: 10.1016/S0140-6736(20)30937-5.
https://doi.org/10.1016/S0140-6736(20)30937-5
[68] F. A. Klok et al., "Incidence of thrombotic complications in critically ill ICU patients with COVID-19," Thromb. Res., no. xxxx, pp. 1-3, 2020, doi: 10.1016/j.thromres.2020.04.013.
https://doi.org/10.1016/j.thromres.2020.04.013
[69] N. R. Madamanchi, Z. S. Hakim, and M. S. Runge, "Oxidative stress in atherogenesis and arterial thrombosis: The disconnect between cellular studies and clinical outcomes," J. Thromb. Haemost., vol. 3, no. 2, pp. 254-267, 2005, doi: 10.1111/j.1538-7836.2004.01085.x.
https://doi.org/10.1111/j.1538-7836.2004.01085.x
[70] N. R. Brady, A. Hamacher-Brady, H. V Westerhoff, and R. A. Gottlieb, "A wave of reactive oxygen species (ROS)-induced ROS release in a sea of excitable mitochondria.," Antioxid. Redox Signal., vol. 8, no. 9-10, pp. 1651-1665, 2006, doi: 10.1089/ars.2006.8.1651.
https://doi.org/10.1089/ars.2006.8.1651
[71] D. B. Zorov, M. Juhaszova, and S. J. Sollott, "Mitochondrial ROS-induced ROS release: an update and review.," Biochim. Biophys. Acta, vol. 1757, no. 5-6, pp. 509-517, 2006, doi: 10.1016/j.bbabio.2006.04.029.
https://doi.org/10.1016/j.bbabio.2006.04.029
[72] E. Prompetchara, C. Ketloy, and T. Palaga, "Immune responses in COVID-19 and potential vaccines: Lessons learned from SARS and MERS epidemic," Asian Pacific J. allergy Immunol., vol. 38, no. 1, pp. 1-9, 2020, doi: 10.12932/AP-200220-0772.
https://doi.org/10.12932/AP-200220-0772
[73] G. T. Nguyen, E. R. Green, and J. Mecsas, "Neutrophils to the ROScue: Mechanisms of NADPH Oxidase Activation and Bacterial Resistance," Front. Cell. Infect. Microbiol., vol. 7, p. 373, Aug. 2017, doi: 10.3389/fcimb.2017.00373.
https://doi.org/10.3389/fcimb.2017.00373
[74] F. Lovren et al., "Angiotensin converting enzyme-2 confers endothelial protection and attenuates atherosclerosis.," Am. J. Physiol. Heart Circ. Physiol., vol. 295, no. 4, pp. H1377-84, Oct. 2008, doi: 10.1152/ajpheart.00331.2008.
https://doi.org/10.1152/ajpheart.00331.2008
[75] Y.-H. Zhang et al., "ACE2 and Ang-(1-7) protect endothelial cell function and prevent early atherosclerosis by inhibiting inflammatory response.," Inflamm. Res., vol. 64, no. 3-4, pp. 253-260, Apr. 2015, doi: 10.1007/s00011-015-0805-1.
https://doi.org/10.1007/s00011-015-0805-1
[76] et al., "Presenting Characteristics, Comorbidities, and Outcomes Among 5700 Patients Hospitalized With COVID-19 in the New York City Area," Jama, vol. 10022, pp. 1-8, 2020, doi: 10.1001/jama.2020.6775.
https://doi.org/10.1001/jama.2020.6775
[77] M. Nozoe et al., "Mitochondria-derived reactive oxygen species mediate sympathoexcitation induced by angiotensin II in the rostral ventrolateral medulla," J. Hypertens., vol. 26, no. 11, p. 2176-2184, Nov. 2008, doi: 10.1097/hjh.0b013e32830dd5d3.
https://doi.org/10.1097/HJH.0b013e32830dd5d3
[78] S. I. Dikalov and Z. Ungvari, "Role of mitochondrial oxidative stress in hypertension.," Am. J. Physiol. Heart Circ. Physiol., vol. 305, no. 10, pp. H1417-27, Nov. 2013, doi: 10.1152/ajpheart.00089.2013.
https://doi.org/10.1152/ajpheart.00089.2013
[79] V. R. Vaka et al., "Blockade of endogenous angiotensin II type I receptor agonistic autoantibody activity improves mitochondrial reactive oxygen species and hypertension in a rat model of preeclampsia.," Am. J. Physiol. Regul. Integr. Comp. Physiol., vol. 318, no. 2, pp. R256-R262, Feb. 2020, doi: 10.1152/ajpregu.00179.2019.
https://doi.org/10.1152/ajpregu.00179.2019
[80] J. Gonzalez, N. Valls, R. Brito, and R. Rodrigo, "Essential hypertension and oxidative stress: New insights.," World J. Cardiol., vol. 6, no. 6, pp. 353-366, Jun. 2014, doi: 10.4330/wjc.v6.i6.353.
https://doi.org/10.4330/wjc.v6.i6.353
[81] R. M. Touyz, G. Yao, M. T. Quinn, P. J. Pagano, and E. L. Schiffrin, "p47phox associates with the cytoskeleton through cortactin in human vascular smooth muscle cells: role in NAD(P)H oxidase regulation by angiotensin II.," Arterioscler. Thromb. Vasc. Biol., vol. 25, no. 3, pp. 512-518, Mar. 2005, doi: 10.1161/01.ATV.0000154141.66879.98.
https://doi.org/10.1161/01.ATV.0000154141.66879.98
[82] C. N. Young, "Endoplasmic reticulum stress in the pathogenesis of hypertension.," Exp. Physiol., vol. 102, no. 8, pp. 869-884, Aug. 2017, doi: 10.1113/EP086274.
https://doi.org/10.1113/EP086274
[83] C. X. C. Santos, A. A. Nabeebaccus, A. M. Shah, L. L. Camargo, S. V Filho, and L. R. Lopes, "Endoplasmic reticulum stress and Nox-mediated reactive oxygen species signaling in the peripheral vasculature: potential role in hypertension.," Antioxid. Redox Signal., vol. 20, no. 1, pp. 121-134, Jan. 2014, doi: 10.1089/ars.2013.5262.
https://doi.org/10.1089/ars.2013.5262
[84] A. S. Fauci, H. C. Lane, and R. R. Redfield, "Covid-19 - Navigating the Uncharted.," The New England journal of medicine, vol. 382, no. 13. United States, pp. 1268-1269, Mar. 2020, doi: 10.1056/NEJMe2002387.
https://doi.org/10.1056/NEJMe2002387
[85] R. E. Jordan, P. Adab, and K. K. Cheng, "Covid-19: risk factors for severe disease and death," BMJ, vol. 368, p. m1198, Mar. 2020, doi: 10.1136/bmj.m1198.
https://doi.org/10.1136/bmj.m1198
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How to Cite
[1]
H. R. Baqi, H. A. M. Farag, A. H. H. El Bilbeisi, R. H. Askandar, and A. M. El Afifi, “Oxidative Stress and Its Association with COVID-19: A Narrative Review”, KJAR, vol. 5, no. 3, pp. 97–105, Jun. 2020, doi: 10.24017/covid.11.
Published
01-06-2020
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Section
Pure and Applied Science
