acetaminophen depletion of glutathione in various organs The Use and Potential Benefits N-Acetylcysteine Non-Acetaminophen Acute Liver Failure: An Etiology-Based Review Acetaminophen – metabolism

doi: 10.1038/s41392-025-02176-0 48 KaloniDDiepstratenSTStrasserAKellyGL

Under normal physiological conditions, neuronal action potentials are transmitted to presynaptic terminals, causing voltage-gated Ca 2+ channels to open and extracellular Ca 2+ to flow in, prompting synaptic vesicles to release glutamate into the synaptic cleft, where glutamate binds to glutamate receptors on the postsynaptic membrane, triggering the influx of cations into the postsynaptic neuron and altering the membrane potential to achieve signal transmission

This is the key observation underlying the importance ascribed to the close redox coupling of ascorbate and glutathione pools in vivo , which allows glutathione to play an indirect role in H 2 O 2 reduction as part of a reaction sequence that ultimately depends on electrons derived from NAD(P)H and/or ferredoxin (Figure 1)

This reasoning fails at three levels