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Such treatments include administration of the GSH precursor, N-acetylcysteine (NAC), and GSH-monoethylester (GSH-MEE), a cell permeable form of GSH, and induction of the transcription factor, nuclear factor erythroid 2-related factor-2 (Nrf2), which is involved in transcriptional regulation of -glutamyl-cysteine ligase, the rate-limiting enzyme necessary for GSH synthesis [19]

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