Stable Nitroxide as Diagnostic Tools for Monitoring of Oxidative Stress and Hypoalbuminemia in the Context of COVID-19

Figures

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  Figure 1. Immune response and redox imbalance during SARS-CoV-2 infection.

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  Figure 2. The flow diagram shows the methodology for selecting articles. This methodology follows the recommendations given in PRISMA-P guideline rules [25] and PRISMA-S named “PRISMA-S: an extension to the PRISMA Statement for Reporting Literature Searches in Systematic Reviews” for reporting literature searches.

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  Figure 3. Inflammation response and hepcidin during SARS-CoV-2 infection. Transported iron into cells (Fe2+) binds to ferritin or is transported into the bloodstream by ferroportin, where it is oxidized to Fe3+. Oxidized iron forms a complex with transferrin, which allows efficient iron transport in the body. The inflammatory response triggers the production of hepcidin, which is part of the body’s defense mechanism against pathogens. During SARS-CoV-2 infection, interleukin-6 (IL-6) induced hepcidin induction via the IL-6R/STAT3 pathway. It leads to high hepcidin levels and, as a result, to inhibiting and decreasing ferroportin activity.

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  Figure 4. Redox reactions of nitroxides: diamagnetic non-radical forms hydroxyl amine (>N-OH), and paramagnetic radical form (>NO•) involvement of the hydroxylamine form of TEMPOL-H in redox reactions in the presence of ROS, in which the emergence of an EPR signal and recovery of the nitroxide radical form is observed.

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  Figure 5. Redox reactions of TEMPOL in the presence of free iron, •OH, and H2O2. Efficiency of the nitroxide radical in metabolizing O2•− and H2O2 or in protecting cells from •OH; TEMPOL sensitivity was found to be the highest for •OH.