There is a possible role for oxidative stress, a state characterized by an altered balance between the production of free radicals or reactive oxygen species (ROS) and antioxidant defences, in coronavirus disease 2019 (COVID-19), the genesis of which is quite complex. Excessive oxidative stress could be responsible for the alveolar damage, thrombosis, and red blood cell dysregulation observed in COVID-19. Apparently, deficiency of glutathione (GSH), a low-molecular-weight thiol that is the most important non-enzymatic antioxidant molecule and has the potential to keep the cytokine storm in check, is a plausible explanation for the severe manifestations and death in COVID-19 patients. Thiol drugs, which are considered mucolytic, also possess potent antioxidant and anti-inflammatory properties. They exhibit antibacterial activity against a variety of medically important bacteria and may be an effective strategy against influenza virus infection. The importance of oxidative stress during COVID-19 and the various pharmacological characteristics of thiol-based drugs suggest a possible role of thiols in the treatment of COVID-19. Oral and intravenous GSH, as well as GSH precursors such as N-acetylcysteine (NAC), or drugs containing the thiol moiety (erdosteine) may represent a novel therapeutic approach to block NF-kB and address the cytokine storm syndrome and respiratory distress observed in COVID-19 pneumonia patients
【저자키워드】 COVID-19, oxidative stress, N-acetylcysteine, Erdosteine, 【초록키워드】 Treatment, coronavirus disease, thrombosis, Infection, drugs, Influenza virus, drug, thiol, antioxidant, NF-kB, Characteristics, ROS, Bacteria, oral, patients, Blood, Therapeutic approach, distress, manifestation, intravenous, dysregulation, alveolar damage, free radical, deficiency, GSH, complex, syndrome, anti-inflammatory properties, precursor, pharmacological, effective, Cell, NAC, responsible, characterized, variety, reactive oxygen specy, COVID-19 pneumonia patient, death in COVID-19, the cytokine storm, 【제목키워드】 thiol, current,