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Reactive oxygen species as an initiator of toxic innate immune responses in retort to SARS-CoV-2 in an ageing population, consider N-acetylcysteine as early therapeutic intervention
| dc.creator | Nasi A., McArdle S., Gaudernack G., Westman G., Melief C., Rockberg J., Arens R., Kouretas D., Sjölin J., Mangsbo S. | en |
| dc.date.accessioned | 2023-01-31T09:03:41Z | |
| dc.date.available | 2023-01-31T09:03:41Z | |
| dc.date.issued | 2020 | |
| dc.identifier | 10.1016/j.toxrep.2020.06.003 | |
| dc.identifier.issn | 22147500 | |
| dc.identifier.uri | http://hdl.handle.net/11615/76922 | |
| dc.description.abstract | During the current COVID-19 pandemic, a need for evaluation of already available drugs for treatment of the disease is crucial. Hereby, based on literature review from the current pandemic and previous outbreaks with corona viruses we analyze the impact of the virus infection on cell stress responses and redox balance. High levels of mortality are noticed in elderly individuals infected with SARS-CoV2 and during the previous SARS-CoV1 outbreak. Elderly individuals maintain a chronic low level of inflammation which is associated with oxidative stress and inflammatory cytokine production, a condition that increases the severity of viral infections in this population. Coronavirus infections can lead to alterations of redox balance in infected cells through modulation of NAD + biosynthesis, PARP function along with altering proteasome and mitochondrial function in the cell thereby leading to enhanced cell stress responses which further exacerbate inflammation. ROS production can increase IL-6 production and lipid peroxidation resulting in cell damage. Therefore, early treatment with anti-oxidants such as NAC during COVID-19 can be a way to bypass the excessive inflammation and cell damage that lead to severe infection, thus early NAC as intervention should be evaluated in a clinical trial setting. © 2020 The Authors | en |
| dc.language.iso | en | en |
| dc.source | Toxicology Reports | en |
| dc.source.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-85086894523&doi=10.1016%2fj.toxrep.2020.06.003&partnerID=40&md5=468c9d26248127bb390cce5617922aea | |
| dc.subject | acetylcysteine | en |
| dc.subject | angiotensin converting enzyme 2 | en |
| dc.subject | C reactive protein | en |
| dc.subject | cryopyrin | en |
| dc.subject | group 2d secretory phospholipase a2 | en |
| dc.subject | inflammasome | en |
| dc.subject | interferon | en |
| dc.subject | interleukin 6 | en |
| dc.subject | neutrophil cytosol factor 1 | en |
| dc.subject | nicotinamide adenine dinucleotide adenosine diphosphate ribosyltransferase | en |
| dc.subject | peptides and proteins | en |
| dc.subject | proteasome | en |
| dc.subject | reactive oxygen metabolite | en |
| dc.subject | reduced nicotinamide adenine dinucleotide phosphate oxidase | en |
| dc.subject | toll like receptor 4 | en |
| dc.subject | tryptophan 2,3 dioxygenase | en |
| dc.subject | tumor necrosis factor | en |
| dc.subject | unclassified drug | en |
| dc.subject | aging | en |
| dc.subject | Article | en |
| dc.subject | cell stress | en |
| dc.subject | coronavirus disease 2019 | en |
| dc.subject | cytokine production | en |
| dc.subject | cytokine release | en |
| dc.subject | homeostasis | en |
| dc.subject | human | en |
| dc.subject | immune response | en |
| dc.subject | innate immunity | en |
| dc.subject | mortality | en |
| dc.subject | nonhuman | en |
| dc.subject | oxidation reduction reaction | en |
| dc.subject | oxidative phosphorylation | en |
| dc.subject | priority journal | en |
| dc.subject | protein expression | en |
| dc.subject | Severe acute respiratory syndrome coronavirus 2 | en |
| dc.subject | viremia | en |
| dc.subject | Elsevier Inc. | en |
| dc.title | Reactive oxygen species as an initiator of toxic innate immune responses in retort to SARS-CoV-2 in an ageing population, consider N-acetylcysteine as early therapeutic intervention | en |
| dc.type | journalArticle | en |
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