Defective Anti-oxidant System: An Aggravating Factor for COVID-19 Patients Outcome?

Kassi, Eva; Papavassiliou, Kostas A.; Papavassiliou, Athanasios G.

doi:10.1016/j.arcmed.2020.05.017

Cited by 10 publications

(8 citation statements)

References 9 publications

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“…Nevertheless, significant alterations in vitamin C, GSH and selenium concentrations, all molecules playing a key role in the immunity, raise questions in the particular framework of the COVID-19 pathogenesis. Associated to increased lipid peroxidation, these observations should therefore create opportunities to explore potential approaches for prevention or treatment by antioxidants, as observed in COVID-19 patients [ 76 , 77 , 78 , 79 , 80 ]. As recently suggested for vitamin C and glutathione [ 33 , 47 , 81 ], monitoring of OSS should be implemented in COVID-19 critically ill patients, including vitamin C, GSH in association with PSH, and, finally, ROOH in association with the Cu/Zn ratio and CRP.…”

Section: Discussionmentioning

confidence: 99%

Oxidative Stress Status in COVID-19 Patients Hospitalized in Intensive Care Unit for Severe Pneumonia. A Pilot Study

et al. 2021

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Background: A key role of oxidative stress has been highlighted in the pathogenesis of COVID-19. However, little has been said about oxidative stress status (OSS) of COVID-19 patients hospitalized in intensive care unit (ICU). Material and Methods: Biomarkers of the systemic OSS included antioxidants (9 assays), trace elements (3 assays), inflammation markers (4 assays) and oxidative damage to lipids (3 assays). Results: Blood samples were drawn after 9 (7–11) and 41 (39–43) days of ICU stay, respectively in 3 and 6 patients. Vitamin C, thiol proteins, reduced glutathione, γ-tocopherol, β-carotene and PAOT® score were significantly decreased compared to laboratory reference values. Selenium concentration was at the limit of the lower reference value. By contrast, the copper/zinc ratio (as a source of oxidative stress) was higher than reference values in 55% of patients while copper was significantly correlated with lipid peroxides (r = 0.95, p < 0.001). Inflammatory biomarkers (C-reactive protein and myeloperoxidase) were significantly increased when compared to normals. Conclusions: The systemic OSS was strongly altered in critically ill COVID-19 patients as evidenced by increased lipid peroxidation but also by deficits in some antioxidants (vitamin C, glutathione, thiol proteins) and trace elements (selenium).

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Section: Discussionmentioning

confidence: 99%

Oxidative Stress Status in COVID-19 Patients Hospitalized in Intensive Care Unit for Severe Pneumonia. A Pilot Study

et al. 2021

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“…It is essential to study whether an intrinsically defective anti-oxidant system, such as G6PD deficiency or other causes, is activated in response to COVID-19 infection [ 109 , 110 ]. Moreover, the use of anti-oxidant therapy may help in inhibiting COVID-19 pathology [ 111 , 112 , 113 ].…”

Section: Oxidative Stress and Apoptosis In Covid-19mentioning

confidence: 99%

Cardiovascular Manifestations of COVID-19 Infection

Magadum

Kishore

2020

Cells

191

136

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SARS-CoV-2 induced the novel coronavirus disease (COVID-19) outbreak, the most significant medical challenge in the last century. COVID-19 is associated with notable increases in morbidity and death worldwide. Preexisting conditions, like cardiovascular disease (CVD), diabetes, hypertension, and obesity, are correlated with higher severity and a significant increase in the fatality rate of COVID-19. COVID-19 induces multiple cardiovascular complexities, such as cardiac arrest, myocarditis, acute myocardial injury, stress-induced cardiomyopathy, cardiogenic shock, arrhythmias and, subsequently, heart failure (HF). The precise mechanisms of how SARS-CoV-2 may cause myocardial complications are not clearly understood. The proposed mechanisms of myocardial injury based on current knowledge are the direct viral entry of the virus and damage to the myocardium, systemic inflammation, hypoxia, cytokine storm, interferon-mediated immune response, and plaque destabilization. The virus enters the cell through the angiotensin-converting enzyme-2 (ACE2) receptor and plays a central function in the virus’s pathogenesis. A systematic understanding of cardiovascular effects of SARS-CoV2 is needed to develop novel therapeutic tools to target the virus-induced cardiac damage as a potential strategy to minimize permanent damage to the cardiovascular system and reduce the morbidity. In this review, we discuss our current understanding of COVID-19 mediated damage to the cardiovascular system.

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“…Recently, different researchers have suggested that oxidative stress in patients with COVID-19 could contribute to cytokine storm and coagulopathy 8 , 9 , 10 , 11 , 12 , 13 , 14 . In vitro studies have found that SARS-CoV-1 infection increases the production of ROS in human promonocyte cells 26 and in various mammalian cells 27 .…”

Section: Discussionmentioning

confidence: 99%

“…Since COVID-19 was declared as a pandemic disease, a large number of investigations have been carried out to better understand its epidemiology, mechanisms, clinical evolution, and management. Recently, several researchers have suggested the potential role of oxidative stress on COVID-19 and it has been proposed that oxidative stress in patients with COVID-19 could contribute in the cytokine storm and coagulopathy; in addition, the use of antioxidants agents has been suggested to reduce oxidative stress 8 , 9 , 10 , 11 , 12 , 13 , 14 .…”

Section: Introductionmentioning

confidence: 99%

DNA and RNA Oxidative Damage and Mortality of Patients With COVID-19

Lorente

Martı́n

González-Rivero

et al. 2021

The American Journal of the Medical Sciences

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Background Deoxyribonucleic acid (DNA) and ribonucleic acid (RNA) oxidative damage is associated with mortality of patients with different diseases. However, there are no data about DNA and RNA oxidative damage from coronavirus disease 2019 (COVID-19) patients. Thus, the objective of this study was to explore DNA and RNA oxidative damage in surviving and non-surviving COVID-19 patients. Methods Eight Intensive Care Units from 6 hospitals in the Canary Islands (Spain) participated in this prospective and observational study. We recorded the serum levels at ICU admission of the three guanine oxidized species (OGS) because guanine is the nucleobase that forms the DNA and RNA most prone to oxidation. Survival at 30 days was our end-point study. Results Non-surviving (n=11) compared to surviving patients (n=42) had higher APACHE-II (p<0.001), SOFA (p=0.004) and serum OGS levels (p=0.001). In logistic regression analyses an association between serum OGS levels and 30-day mortality after controlling for SOFA (OR=2.601; 95% CI=1.305-5.182; p=0.007) or APACHE-II (OR=2.493; 95% CI=1.274-4.879; p=0.008) was found. The area under curve (AUC) for mortality prediction by serum OGS levels was 83% (95% CI=70-92%; p<0.001), by APACHE II was 85% (95% CI=75-96%; p<0.001), and by SOFA was 80% (95% CI=66-94%; p<0.001). No significant differences were found in the AUC between serum OGS levels and SOFA (p=0.91), and serum OGS levels and APACHE-II (p=0.64). Conclusions To our knowledge, this is the first study reporting on oxidative DNA and RNA damage in COVID-19 patients, and the main new finding was that serum OGS concentration was associated with mortality.

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Defective Anti-oxidant System: An Aggravating Factor for COVID-19 Patients Outcome?

Cited by 10 publications

References 9 publications

Oxidative Stress Status in COVID-19 Patients Hospitalized in Intensive Care Unit for Severe Pneumonia. A Pilot Study

Oxidative Stress Status in COVID-19 Patients Hospitalized in Intensive Care Unit for Severe Pneumonia. A Pilot Study

Cardiovascular Manifestations of COVID-19 Infection

DNA and RNA Oxidative Damage and Mortality of Patients With COVID-19

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