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Inhibitor concentration and pre- and co-treatment protocols must be empirically determined based on cell density, duration of exposure, and unique drug-drug interactions

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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

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Yet, we observed that dexamethasone treatment led to reduced tubular injury in vivo, demonstrating the importance of the iron-dependent anti-ferroptotic dexamethasone effects