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Studies have shown that after experimental brain trauma in rats, the production of lipid peroxidation products is significantly enhanced, the consumption of GSH and ascorbic acid is significantly increased (Bayir et al., 2002), and the activity of GPX is decreased (Xu et al., 2014)

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Given this wide-ranging protective role, low levels of glutathione have been shown to be incompatible with optimum health

Variability in NFE2L2 and KEAP1 mutations, coupled with nongenetic mechanisms such as p62/SQSTM1 accumulation, results in highly variable NRF2 activity across tumors, complicating the unification of therapeutic approaches [5, 56]