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We observed that both APR-017 and LCS3 reduced the viability of VRK2-KO cells, but not VRK2-WT cells (Fig

2.8.2 Quantitative proteomic analysis Following enzymatic digestion and desalting, 100 g of protein samples were subjected to LC-MS/MS analysis

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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