Abstract
COVID-19 patients have a higher risk of developing inflammatory responses associated with serious and even fatal respiratory diseases. The role of oxidative stress in exacerbating manifestations in COVID-19 pathogenesis is under-reported.This study aimed touseserum levels of superoxide dismutase (SOD3) and glutathione-S-transferase (GSTp1) by ELISA, zinc (ErbaChem5), ferritin and free iron (VitrosChemistry, Ortho Clinical Diagnosis, Raritan, NJ, USA) at the first encounter of randomly selected RT-PCR-positive COVID-19 patients, for assessing disease severity. The parameters which helped in identifying the severity, leading to poor prognosis, were neutrophil:lymphocyte higher than 4, high CRP, low SOD3 values and high GSTp1 values, and diabetes mellitus as a co-morbidity. Higher zinc levels correlated with high GSTp1 and low SOD3, indicating the protective effect of zinc on ROS. The increased high GSTp1 shows an anticipated protective biochemical response, to mitigate the low SOD3 values due to ROS consumption. Decreased SOD3 levels indicate a state of high oxidative stress at cellular levels, and an anticipated increase in GSTp1 levels points to the pathophysiological bases of increasing severity with age, sex, and co-morbidities, such asdiabetes. High levels of initial GSTp1 and zinc levels possibly offer protection to redox reactions at the cellular level in severe COVID-19 infection, preventing deterioration.
Highlights
SARS-CoV-2 reminds us of the devastating effects of immune dysregulation, following a possible cytokine storm, blood clotting, and exacerbation of hypoxia—a life-threatening systemic inflammatory syndrome involving elevated levels of circulating cytokines and the hyperactivation of immune cells, which can be triggered by various pathogens, autoimmune conditions, and some drug therapies
In states where free radicals are high, such as in COVID-19 [3], the increased production of reactive oxygen species (ROS) or decreased antioxidants may contribute to the worsening of symptoms, resulting in acute respiratory distress syndrome (ARDS) and multi-organ dysfunction syndrome (MODS) [4]
Pulmonary dysfunction and other MODS that occur after a COVID-19 cytokine storm might be the result of enhanced oxidative stress and innate immune activation working in tandem
Summary
SARS-CoV-2 reminds us of the devastating effects of immune dysregulation, following a possible cytokine storm, blood clotting, and exacerbation of hypoxia—a life-threatening systemic inflammatory syndrome involving elevated levels of circulating cytokines and the hyperactivation of immune cells, which can be triggered by various pathogens, autoimmune conditions, and some drug therapies The recognition that such an immune response to the pathogen by our own body, and not the pathogen itself, will result in a multi organ dysfunction has directed our attention to the role of triggering factors which mediate cytokine release. Massive oxidative burst is utilized by the immune cells to kill the invading pathogens This excessive production of ROS has been demonstrated to have a direct destructive effect on the surrounding cells, resulting in direct lung injury in COVID-19 infection [6]. Excessive ROS generation can affect the RBC membrane, resulting in its phagocytosis by macrophages and neutrophil [7]
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