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High levels of glutathione (GSH) are observed in the majority of tumors, contributing to cancer progression and treatment resistance in part by preventing glutathione peroxidase 4dependent (GPX4-dependent) ferroptosis

Generally, for maintaining GSH homeostasis in brain, there are at least two possible mechanisms: (i) glutathione constituents (cysteine moieties) may be recovered and recycled during the turnover of GSH in the brain, and (ii) precursors for brain glutathione synthesis (cysteine, cysteine-containing molecules) might be transported across the blood-brain barrier [13]

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