1 INTRODUCTION
COVID-19 is a viral infection induced by the coronavirus of severe respiratory syndrome (SARS-CoV-2), that represents a serious health problem worldwide; due to its association with various pathophysiological processes such as: inflammation, increased proinflammatory cytokines, and cell death, which could be closely related to redox imbalance or oxidative stress.1 The high risk of severity and mortality from SARS-CoV-2 infection or COVID-19 disease has been associated with several clinical indicators such as: lymphocytopenia, increased D-dimer, increased serum ferritin, and high titers IL-6.1,2
The inflammatory response induced by SARS-CoV-2 can generate an effect of cellular oxidative stress, which induces an increase in circulatory inflammatory mediators, including cytokines, produced through redox pathway activation in patients with sepsis.3,4Because, oxidative stress and inhibition of mitochondrial activity may be an alternative to explain the tissue injury associated with COVID-19-induced damage to endothelial, alveolar, and cardiac cells, among other.5,6 We consider it vitally important that health professionals can analyze and understand a little more about these pathophysiological mechanisms, to evaluate and design new protocols that allow a better prognosis for patients.
According to tissue damage, accumulation of inflammatory cells associated with endothelial tissue has been reported, as well as apoptotic bodies in alveolar cells and others.7 Thus, it is postulated the accumulation of mononuclear cells in the lung and in the small pulmonary vessels induce congestion and therefore endothelial tissue damage associated with the lung.8The endothelial dysfunction is a main determinant of microvascular dysfunction, which is associated with the processes of inflammation and oxidative stress, that potentiate tissue edema associated with a pro-coagulant state.6,9
The SARS-CoV-2 induce an explosion of inflammatory cytokines, reactive oxygen species (ROS), and cell death-induced by this cell events is a cause which can result in significant endothelial and multi-organ damage, so the regulation of oxidative stress is essential.3,4,7 Thus, modulation of oxidative stress may be able to prevent the cellular and tissue injury and development severe disease symptoms in coronavirus patients by reduce the immuno-pathology of coronavirus infection on patients’ health after the active phase of the infection is over, so that, if we could reduce or modulate cellular toxic effects, it would make COVID-19 disease more controllable.9,11
Therefore, this study aimed to evaluate the association between different biomarkers of oxidative stress with parameters of mitochondrial and cellular function to evaluate the relationship between oxidative stress and leukocyte function in patients with COVID-19. This process contributes to the understanding of the possible link between oxidative stress and the risk of pathogenesis, severity and mortality in patients affected by SARS-CoV-2 infection.