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It follows that UCP2 gene variants associated with lower UCP2 protein levels, and therefore less protection against ROS and oxidative stress, could also be linked to these cardiometabolic diseases

Flachs, P., Rossmeisl, M., Kuda, O

The development of an APAP-induced DILI mouse model based on the mechanism by which N-acetyl-p-benzoquinone imine (NAPQI), a reactive metabolite of APAP, induces hepatotoxicity by depleting GSH, led to the discovery of the antidote N-acetylcysteine (NAC), which has been used clinically for over four decades [91]

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