Pathobiochemical pathways of redox imbalance in the neurological long-term effects of COVID-19 and the role of chondroitin sulfate in the redox status restoration

Abstract

The review examines the epidemiology and clinical manifestations of COVID-19 long-term neurological effects, main pathobiochemical mechanisms, and integrated circuits of redox status impairment in COVID-19, such as the decrease of adenosine triphosphate production, fatty acids levels, acylcarnitine, and amino acids, impairment of oxidative phosphorylation and glycolysis, hypometabolic state, redox imbalance with the increase of peroxides and superoxides, isoprostanes, the decrease of α-tocopherol, substances reacting with thiobarbituric acid, increased nitrosative stress with the increase of inducible synthase of nitric oxide, nitric oxide, peroxynitrite, and nitrate. Neuroprotective approaches aimed at suppressing excitotoxicity, oxidative stress, and neuroinflammation are presented. Recent data on the relationship between mechanisms of chondroitin sulfate and its derivatives (chondroitin sulfate glycoprotein disaccharide) neuroprotective effects and characteristics of their chemical structure are analyzed. The mechanism of action and neuroprotective effects of chondroitin sulfate and its derivatives in fatigue syndrome in patients with SARS-CoV2 infection are discussed (regulation of the PKC/PI3K/Akt activity, the increase of heme oxygenase-1 level, the decrease of reactive oxygen species). The position that chondroitin sulfate and its derivatives can become promising drugs to prevent the long-term neurological effects of COVID-19 is reasoned.