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demonstrated that some of the GSH content was oxidized readily and removed from circulation with a half-time of 10 minutes following an intravenous injection, and the remainder was split to three amino acid components [10]

Once the hepatotoxicity due to APAP was recognized, the mechanisms behind this were extensively investigated, especially in the mouse model, which recapitulates key mechanistic aspects of liver injury in humans such as mitochondrial dysfunction [5,6]

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