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doi: 10.1172/jci.insight.159863, 82 KonanurV

Often yes, such as modifier 25

Mitchell and colleagues showed that, whilst the major routes of biotransformation for APAP are indeed detoxication reactions, that form the phenolic sulfate and glucuronide conjugates, a minor route was the oxidative metabolism of the drug via the P450 system to an electrophilic intermediate, most likely N -acetyl- p -benzoquinoneimine (NAPQI, also commonly termed NABQI), which rapidly depleted hepatic glutathione (GSH).5 Subsequently, it was shown that acetaminophen can be activated by non-P450-dependent metabolism, for example by cyclooxygenases6 and myeloperoxidases,7 although the contribution of this to the toxicity of APAP is unclear