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explored how HGs ability to act on oxidative stress, inflammation, and apoptosisall common in TBI, stroke, and neurodegenerative diseasessuggest therapeutic potential in mitigating the damage caused by brain injuries, improving recovery, and reducing the long-term effects of these conditions [36]

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Selenocysteine-mediated backbone cyclization of unprotected peptides followed by alkylation, oxidative elimination or reduction of the selenol

Re- cent experimental evidence using 16 different cell lines demonstrated that ~0.51% of the GSH pool was associated with proteins when the GSH/GSSG is ~100 and decreasing this ratio with oxidants induced a ~50% increase in the total number of protein glutathionyl adducts [ 18 ]

Future research is likely to focus on enhancing astrocytic support for neuronal GSH levels, particularly in aging and neurodegeneration: strategies may include activating Nrf2-mediated antioxidant responses to upregulate cystine/glutamate antiporter (Sxc ) and glutamine synthetase in astrocytes, or targeting AMPK/SIRT1 pathways to facilitate GSH precursor transfer to neurons