Under normal circumstances, acetaminophen is metabolized in the liver, where it is primarily converted to non-toxic metabolites through glucuronidation and sulfation. A small fraction is converted to a toxic metabolite, N-acetyl-p-benzoquinone imine (NAPQI), which is detoxified by glutathione. In an overdose, the liver's supply of glutathione can become depleted, leading to accumulation of NAPQI, which binds to cellular proteins and causes hepatocellular damage.
