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GSH augmentation as a potential therapeutic strategy in CNS disease has been suggested for decades, 23 although repletion efforts have been hindered by inability to assess human CNS GSH concentrations in vivo and poor oral absorption of GSH
PGE-2, prostaglandin E2
Enzyme activities and subcellular localization of members of the Arabidopsis glutathione transferase superfamily
69 MooneyLAPereraFPVan BennekumAMBlanerWSKarkoszkaJCoveyLet al
R.ChenH.ChipotC.KohlmeyerA.et al (2024)
