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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

The National Cancer Institute conducted chemoinformatics analysis of 60 cell lines and showed a negative correlation between xCT expression levels and sensitivity to compounds associated with GSH-mediated resistance, which indicated that xCT expression induces chemoresistance via GSH-mediated ROS detoxification activity (82)