N-Acetylcysteine: A potential therapeutic agent for SARS-CoV-2

Poe, Francis L.; Corn, Joshua

doi:https://doi.org/10.1016/j.mehy.2020.109862

N-Acetylcysteine: A potential therapeutic agent for SARS-CoV-2

dc.creator	Poe, Francis L.
dc.creator	Corn, Joshua
dc.date.accessioned	2020-07-15T01:49:13Z
dc.date.available	2020-07-15T01:49:13Z
dc.date.created	2020-10
dc.description.abstractenglish	COVID-19, a respiratory disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), continues to spread across the globe. Predisposing factors such as age, diabetes, cardiovascular disease, and lowered immune function increase the risk of disease severity. T cell exhaustion, high viral load, and high levels of TNF-ɑ, IL1β, IL6, IL10 have been associated with severe SARS-CoV-2. Cytokine and antigen overstimulation are potentially responsible for poor humoral response to the virus. Lower cellular redox status, which leads to pro-inflammatory states mediated by TNF-ɑ is also potentially implicated. In vivo, in vitro, and human clinical trials have demonstrated N-acetylcysteine (NAC) as an effective method of improving redox status, especially when under oxidative stress. In human clinical trials, NAC has been used to replenish glutathione stores and increase the proliferative response of T cells. NAC has also been shown to inhibit the NLRP3 inflammasome pathway (IL1β and IL18) in vitro, and decrease plasma TNF-ɑ in human clinical trials. Mediation of the viral load could occur through NAC’s ability to increase cellular redox status via maximizing the rate limiting step of glutathione synthesis, and thereby potentially decreasing the effects of virally induced oxidative stress and cell death. We hypothesize that NAC could act as a potential therapeutic agent in the treatment of COVID-19 through a variety of potential mechanisms, including increasing glutathione, improving T cell response, and modulating inflammation. In this article, we present evidence to support the use of NAC as a potential therapeutic agent in the treatment of COVID-19.	spa
dc.format.extent	4 páginas	spa
dc.format.mimetype	application/pdf	spa
dc.identifier.doi	https://doi.org/10.1016/j.mehy.2020.109862	spa
dc.identifier.issn	0306-9877	spa
dc.identifier.other	https://www.sciencedirect.com/science/article/pii/S0306987720308811?via%3Dihub	spa
dc.identifier.uri	https://hdl.handle.net/20.500.12010/10535
dc.publisher	Science Direct	eng
dc.rights.accessrights	info:eu-repo/semantics/openAccess	spa
dc.source	reponame:Expeditio Repositorio Institucional UJTL	spa
dc.source	instname:Universidad de Bogotá Jorge Tadeo Lozano	spa
dc.subject	Agotamiento de células T	spa
dc.subject.keyword	COVID-19	spa
dc.subject.keyword	SARS-COV-2	spa
dc.subject.keyword	Coronavirus	spa
dc.subject.keyword	N-acetylcysteine	spa
dc.subject.keyword	NAC	spa
dc.subject.keyword	Glutathione	spa
dc.subject.keyword	NLRP3	spa
dc.subject.keyword	T Cell Exhaustion	spa
dc.subject.keyword	TNF-ɑ	spa
dc.subject.keyword	Oxidative stress	spa
dc.subject.keyword	Redox status	spa
dc.subject.keyword	Redox potential	spa
dc.subject.lemb	Síndrome respiratorio agudo grave	spa
dc.subject.lemb	COVID-19	spa
dc.subject.lemb	SARS-CoV-2	spa
dc.subject.lemb	Coronavirus	spa
dc.title	N-Acetylcysteine: A potential therapeutic agent for SARS-CoV-2	spa
dc.type.hasversion	info:eu-repo/semantics/acceptedVersion	spa
dc.type.local	Artículo	spa

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