The Impact of Severe COVID-19 on Plasma Antioxidants

Abstract

Several studies suggested the association of COVID-19 with systemic oxidative stress, in particular with lipid peroxidation and vascular stress. Therefore, this study aimed to evaluate the antioxidant signaling in the plasma of eighty-eight patients upon admission to the Clinical Hospital Dubrava in Zagreb, of which twenty-two died within a week, while the other recovered. The differences between the deceased and the survivors were found, especially in the reduction of superoxide dismutases (SOD-1 and SOD-2) activity, which was accompanied by the alteration in glutathione-dependent system and the intensification of the thioredoxin-dependent system. Reduced levels of non-enzymatic antioxidants, especially tocopherol, were also observed, which correlated with enhanced lipid peroxidation (determined by 4-hydroxynonenal (4-HNE) and neuroprostane levels) and oxidative modifications of proteins assessed as 4-HNE-protein adducts and carbonyl groups. These findings confirm the onset of systemic oxidative stress in patients with severe SARS-CoV-2, especially those who died from COVID-19, as manifested by strongly reduced tocopherol level and SOD activity associated with lipid peroxidation. Therefore, we propose that preventive and/or supplementary use of antioxidants, especially of lipophilic nature, could be beneficial for the treatment of COVID-19 patients.

Alterations of the Antioxidant and Inflammatory Response of the Peripheral Blood Granulocytes to SARS-CoV-2 Infection in the Deceased COVID-19 Patients

“…However, given the observed results of the Nrf2 antioxidant response in the lung biopsies of COVID-19 patients, which indicate the suppression of genes associated with the Nrf2 antioxidant response, and in vitro experiments that have shown that the expression of Nrf2 inducible proteins is also reduced, it is likely that the suppression of this metabolic pathway occurs in COVID-19 patients [41]. These data are in agreement of the decreased SOD1 and SOD2 activities observed in current study, reflecting also decrease of the SOD levels recently revealed in the plasma of COVID-19 patients [43]. In contrast, the inverse granulocyte response to COVID-19 with respect to HO-1 may be a specific gene response of that protein or the type of cell whose antioxidant response was analyzed.…”

Selenium Status and Oxidative Stress in SARS-CoV-2 Patients

“…In another study, to determine the relationship between COVID-19 and oxidative stress (vascular stress and lipid peroxidation), the authors demonstrated that there was a reduction in antioxidant capacity, and thus, the patients were unable to counteract oxidative modifications [ 37 , 38 ]. Moreover, our results are consistent with previous studies indicating that oxidative stress markers are significantly elevated in COVID-19 patients.…”

“…This research is critical because it helps to understand the interventions that can be incorporated to reduce adverse outcomes, such as the potential of developing other adverse conditions during high viral load, such as in the case of COVID-19. For instance, Žarković suggested how to respond to patients with SARS-CoV-2 by administering antioxidants such as lipophilic agents that can help to counter the spread of the virus [ 38 ]. Furthermore, Chavarría et al established that antioxidant therapy can help to reduce the severity of conditions such as COVID-19 because it improves the survival rates of critical outcomes such as sequential organ failure assessment (SOFA) [ 27 ].…”

Role of different types of RNA molecules in the severity prediction of SARS-CoV-2 patients

“…Few important biological functions related to selected features in severity prediction with reasonable p-value are floor plate formation, alpha-2B adrenergic receptor binding [35] , thymus development [21] , [48] , positive regulation of histone modification and chromatin organization [4] , [77] , [96] , nephron tubule epithelial cell differentiation [112] , HMG box domain binding [40] , [41] , [97] , platelet formation and morphogenesis [10] , [64] , [83] , positive regulation/regulation of memory T cell activation [45] , [66] , interleukin-4-dependent isotype switching to IgE isotypes, response to nitrogen dioxide [119] , [47] , [69] , axon part and terminus, neuron projection terminus, synapse, mesonephric tubule formation, metanephric mesenchyme development [107] , syntaxin-1 binding [81] , stereocilia ankle link complex, regulation of actin phosphorylation, aminophospholipid transport [9] , positive regulation of long term synaptic depression [13] , [73] , nuclear RNA export factor complex [46] , motor neuron apoptotic process, positive regulation of norepinephrine secretion [61] , cellular response to lipid hydroperoxide [117] , [60] , modified amino acid binding, PCSK9-AnxA2 complex, glutathione binding [103] , [28] , [53] , oligopeptide binding [3] , [58] , metalloendopeptidase inhibitor activity, glutathione derivative metabolic [28] and biosynthetic process [36] , mesonephric tubule formation, zymogen granule, nephron tubule epithelial cell differentiation and negative regulation of regulatory T cell differentiation [105] .…”