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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) (Hanawa et al., 2008

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Researchers investigate its role as a cofactor for glutathione peroxidase and S-transferase enzymes, and examine its involvement in xenobiotic metabolism and heavy metal chelation pathways in cell cultures

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