Protection Against Oxidative Stress as an Important Therapeutic Factor in Pandemic Coronavirus Infection

Abstract

This short article discusses protection against oxidative stress as an additional therapeutic factor in coronavirus infection. The authors describe oxidative stress in the virus host as the predominance of free radicals over antioxidants and state that free radicals oxidatively damage lipids, proteins, nucleic acids and carbohydrates, which they link to the virus obtaining energy for reproduction, and that oxidation of nitrogenous bases causes mutations that allow the virus to resist vaccines. They point to the danger of a combined “free radical storm” and cytokine storm, the vulnerability of the lungs, which usually lack glutathione, and a lack of vitamin D3 and other antioxidants. Malondialdehyde produced by lipoperoxidation is described as binding to proteins such as immunoglobulins, which then lose their antiviral activity. The authors propose that mutations could be prevented by small molecules of selenite or iodide, and mention acetyl-CoA, sirtuins, blocking lipid synthesis with fenofibrate, antioxidants with a low redox potential and senolytics that remove senescent cells. They note that total antioxidant capacity drops with age, putting seniors at greater risk, and that oxidative stress also occurs in other viral diseases. They conclude that reducing oxidative stress, malondialdehyde formation and lipoperoxidation, and preventing virus mutations, should be considered as an additional therapy against the coronavirus.

Abstract prepared by the editorial office from the full text of the article; the authors did not supply one.