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The primary reasons behind the use of N-acetylcysteine over pure glutathione as a therapeutic strategy include the low bioavailability and short half-life (2 min) of glutathione when administered orally or intravenously [16,105]

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In contrast to the transport of GSH in kidney mitochondria, which occurs with a single kinetic component (21), the kinetics of GSH in rat liver mitochondria displays a high-affinity and a low-affinity component (25, 96)