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Therefore, considering the presence of APAP protein adducts at the therapeutic dose of APAP, formation of protein adducts on mitochondrial proteins rather than the overall formation of protein adducts may be the reason for cellular toxicity, which has been considered a key factor for necrotic cell death in previous years ( Depleted glutathione by NAPQI leads to increased H 2 O 2 release that oxidizes thioredoxin and induces the disassociation of thioredoxin from apoptosis signalling-regulating kinase 1 (ASK-1), triggering self-activation of ASK-1, which phosphorylates mitogen-activated protein kinase kinase 4/7 and activates c-Jun N-terminal kinase (JNK) (Win et al., 2016)

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Gastroenterology 162:1088–97.e3 [DOI] [PubMed] [Google Scholar] 45.Fontana L, Partridge L, Longo VD