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10.1016/j.mehy.2020.109862 http://scihub22266oqcxt.onion/10.1016/j.mehy.2020.109862 32504923!7261085!32504923     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Med+Hypotheses 2020 ; 143 (ä): 109862 Nephropedia Template TP {{tp|p=32504923|t=2020. N-Acetylcysteine: A potential therapeutic agent for SARS-CoV-2 |pdf=|usr=}}{{32504923}} gab.com Text N-Acetylcysteine: A potential therapeutic agent for SARS-CoV-2 JO: Med Hypotheses http://www.kidney.de/pget.php?&tw=1&pmid=32504923 #FOAvip 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-a, IL1beta, 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-a 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 (IL1beta and IL18) in vitro, and decrease plasma TNF-a 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. Twit Text FOAVip N-Acetylcysteine: A potential therapeutic agent for SARS-CoV-2 ????Med Hypotheses http://www.kidney.de/pget.php?&tw=1&pmid=32504923 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32504923 #FOAvip English Wikipedia <ref>{{Cite pmid|32504923}}</ref> N-Acetylcysteine: A potential therapeutic agent for SARS-CoV-2 #MMPMID32504923 Poe FL; Corn J Med Hypotheses 2020[Oct]; 143 (ä): 109862 PMID32504923show ga 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-a, IL1beta, 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-a 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 (IL1beta and IL18) in vitro, and decrease plasma TNF-a 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. |Acetylcysteine/*therapeutic use[MESH] |Betacoronavirus[MESH] |COVID-19[MESH] |COVID-19 Drug Treatment[MESH] |Clinical Trials as Topic[MESH] |Coronavirus Infections/*drug therapy[MESH] |Free Radicals[MESH] |Glutathione[MESH] |Humans[MESH] |Inflammation[MESH] |NLR Family, Pyrin Domain-Containing 3 Protein/metabolism[MESH] |Oxidation-Reduction[MESH] |Oxidative Stress[MESH] |Pandemics[MESH] |Pneumonia, Viral/*drug therapy[MESH] |SARS-CoV-2[MESH] |Severe Acute Respiratory Syndrome[MESH] |T-Lymphocytes/drug effects/virology[MESH] |Tumor Necrosis Factor-alpha/metabolism[MESH]N-Acetylcysteine: A potential therapeutic agent for SARS-CoV-2 (epmc).pdf DeepDyve Pubget Overpricing