2021
DOI: 10.1016/j.ijbiomac.2021.08.095
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Review on oxidative stress relation on COVID-19: Biomolecular and bioanalytical approach

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Cited by 24 publications
(14 citation statements)
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References 241 publications
(284 reference statements)
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“…However, what defines the disease’s progression is not entirely understood. Still, there are strong indications that oxidative stress and the defense against reactive oxygen species (ROS) are crucial in COVID-19 pathogenesis on various mechanistic levels [ 13 ]. Upon the binding of SARS-CoV-2 Spike (S) protein to the ACE2 receptor on the cell membrane, the virus enters the cell by endocytosis, leading to RNA replication and translation of viral structural proteins, such as Spike (S), Nucleocapsid (N), Membrane (M), Envelope (E), as well as viral open reading frames (ORFs) and activation of oxidative stress and inflammatory pathways.…”
Section: Introductionmentioning
confidence: 99%
“…However, what defines the disease’s progression is not entirely understood. Still, there are strong indications that oxidative stress and the defense against reactive oxygen species (ROS) are crucial in COVID-19 pathogenesis on various mechanistic levels [ 13 ]. Upon the binding of SARS-CoV-2 Spike (S) protein to the ACE2 receptor on the cell membrane, the virus enters the cell by endocytosis, leading to RNA replication and translation of viral structural proteins, such as Spike (S), Nucleocapsid (N), Membrane (M), Envelope (E), as well as viral open reading frames (ORFs) and activation of oxidative stress and inflammatory pathways.…”
Section: Introductionmentioning
confidence: 99%
“…NOX2-mediated excessive ROS production in endothelial cells generated by SARS-CoV-2 infection combined with a dysregulation and/or extremely exaggerated immune imbalance (so-called cytokine response or cytokine storm) might be among the most important mechanisms of endothelial cell injury during COVID-19 [ 16 , 17 ]. This phenomenon successively aggravates disease progression, activates immune and endothelial cells and platelets, as well as vigorous endothelial inflammatory reactions, which may cause oxidative stress (OS), leading to inflammatory injury and vascular thrombosis and possibly driving ARDS (acute respiratory distress syndrome) or multi-organ failure, pulmonary edema, and, ultimately, mortality [ 18 , 19 , 20 , 21 ]. Oxidative stress (OS) can be induced by different viruses and infections, such as influenza [ 22 ], human respiratory syncytial virus [ 23 ], and rhinoviruses [ 24 ], which employ diverse mechanisms in the human body/organism and may profoundly impact COVID-19 pathogenesis.…”
Section: Introductionmentioning
confidence: 99%
“…In addition, it neutralizes the damage caused by viral infections, through interactions with a number of cellular proteins, signaling molecules and enzymes [14]. Natural antioxidants can compensate for the modified signaling pathways that are activated during the pathogenesis of COVID-19 [15]. The superoxide anion (O 2− ), hydroxyl radical (OH − ), hydrogen peroxide (H 2 O 2 ), hypochlorous acid (HOCl) and also NADPH oxidase-derived ROS are correlated with inflammation [16].…”
Section: Introductionmentioning
confidence: 99%