ZhangNYLiuJYZhengHWangKMZhangJMengNet al
We observed that both APR-017 and LCS3 reduced the viability of VRK2-KO cells, but not VRK2-WT cells (Fig
10.1016/j.canlet.2018.05.036 132 LiL.AggarwalB
Ayfer AytemurZBaysakAOzdemirOKseTSayinerA
Stable and controllable RNA interference: investigating the physiological function of glutathionylated actin
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
