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Neuroinflammation Neuroinflammation is increasingly recognized as a key factor interacting with neurobiological correlates of the neuropsychiatric long COVID syndrome, such as brain serotonin depletion [111], hypothalamicpituitaryadrenal (HPA) axis dysregulation [57], and impaired hippocampal neurogenesis and plasticity [13, 61]
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Using SAL1 recombinant protein treated with reduced or oxidized forms of DTT and glutathione, it appeared that Cys119 is involved in an intermolecular disulfide bridge that led to the formation of a dimeric form and that this would favor the formation of an additional intramolecular disulfide bridge between Cys167 and Cys190 ( In vitro glutathionylation with GSSG leads to glutathionylation of Cys119 and to the formation of the Cys167Cys190 intramolecular disulfide ( Redox regulation at the level of the primary sulfur metabolic pathway Sulfite reductase is a 70 kDa enzyme that catalyzes the reduction of sulfite into sulfide
