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Indeed, it was recently reported that treatment of cells with H 2 O 2 , which can lower GSH levels, leads to increased expression of NRF2 target genes in a KEAP1-independent mechanism 69
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FIGURE 4 This is complicated because as a polar, charged tripeptide, transport of GSH is significantly inhibited by the blood-brain barrier (BBB), thus limiting effective delivery to brain-resident immune cells such as microglia which are central drivers of neuroinflammatory pathology ( As many treatments for neurological conditions have been hampered by limited permeability of the BBB, significant emphasis has been placed on research directed towards advanced drug delivery methods ( More targeted CNS uptake has been attempted by conjugating polymeric nanoparticles with ligands like transferrin or lactoferrin ( As a combined medicinal treatment for viral infections such as COVID-19 or influenza, administration of GSH or NAC in conjunction with established anti-viral treatment has been found to improve lymphocyte response, reduce pro-inflammatory cytokines and reduce cellular oxidative injury ( As a pharmacologic therapeutic, optimizing the efficacy of GSH and minimizing its unintended effects means it is crucial to determine the correct timing, dose, and disease context ( In addition to being a therapeutic target, oxidative stress has been shown to decrease the GSH:GSSG ratio which has proven useful as a clinically accessible, pharmacodynamic biomarker of immune redox tone for conditions such as malignancy (Zitka et al., 2012)
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