How to Restore Oxidative Balance That Was Disrupted by SARS-CoV-2 Infection.
Kajetan KiełbowskiMariola HerianAndrzej PawlikPublished in: International journal of molecular sciences (2022)
Coronavirus 2019 disease (COVID-19) is caused by different variants of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) which emerged in December of 2019. COVID-19 pathogenesis is complex and involves a dysregulated renin angiotensin system. Severe courses of the disease are associated with a dysregulated immunological response known as cytokine storm. Many scientists have demonstrated that SARS-CoV-2 impacts oxidative homeostasis and stimulates the production of reactive oxygen species (ROS). In addition, the virus inhibits glutathione (GSH) and nuclear factor erythroid 2-related factor 2 (NRF2)-a major antioxidant which induces expression of protective proteins and prevents ROS damage. Furthermore, the virus stimulates NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasomes which play a significant role in inducing a cytokine storm. A variety of agents with antioxidant properties have shown beneficial effects in experimental and clinical studies of COVID-19. This review aims to present mechanisms of oxidative stress induced by SARS-CoV-2 and to discuss whether antioxidative drugs can counteract detrimental outcomes of a cytokine storm.
Keyphrases
- respiratory syndrome coronavirus
- sars cov
- oxidative stress
- coronavirus disease
- reactive oxygen species
- nuclear factor
- dna damage
- anti inflammatory
- cell death
- toll like receptor
- diabetic rats
- induced apoptosis
- ischemia reperfusion injury
- poor prognosis
- drug induced
- copy number
- early onset
- type diabetes
- gene expression
- small molecule
- amino acid
- endoplasmic reticulum stress
- insulin resistance
- disease virus