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Acetaminophen toxicity arises from the formation of the reactive metabolite N-acetyl-p-benzoquinone imine (NAPQI). When glutathione (GSH) stores are depleted, NAPQI covalently binds to hepatic proteins, particularly mitochondrial proteins, resulting in protein dysfunction, oxidative stress, cell death, and liver injury. The resulting acetaminophen-protein adducts are clinically relevant biomarkers for APAP-induced liver injury.
N/A - This is a consequence of acetaminophen metabolism and protein binding, not a direct drug target.
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