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Although further clinical evidences are still needed for elucidating the precise mechanism, it is considered plausible that EAAC1 dysfunction leading to GSH depletion is closely involved in neurodegenerative diseases

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Gure, 1998

As demonstrated in egtA 26933 , abrogation of EGT biosynthesis resulted in a shift in the redox state of the cell, which required the alteration of gliotoxin and GSH biosynthesis to compensate (Figure 5)