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This process is non-specific and can lead to the hyper-glutathionylation of proteins, altering their activity

5) and can be started regardless of the type of enzyme deficiency underlying the urea cycle [38, 39], the goal of treatment being to reduce ammonia production and accelerate elimination via alternative pathways (Fig

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RomOLiuYFinneyACGhrayebAZhaoYShukhaYet alInduction of glutathione biosynthesis by glycine-based treatment mitigates atherosclerosis