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However, when the level of APAP overwhelms the primary glucuronidation pathway, the GSH stores are consumed by a generation of the excess NAPQI metabolites and by the formation of mitochondrial NAPQI protein adducts, leading to hepatocellular injury [243]

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This finding reframed the aging-GSH relationship: the bottleneck is not the synthesis machinery itself but the substrate supply, which has practical implications for supplementation strategy