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. 2016 Jun 15;4(2):131–142. doi: 10.14218/JCTH.2015.00052

Table 3. Role of NAC.

1 Protection against reactive oxygen species by increasing Nrf2 and HO-1 mRNA levels
2 Protection against mitochondrial dysfunction, which causes release of acylcarnitines in peripheral vasculature
3 Elimination of JNK activation and GDH release
4 The mechanism of protection during the early metabolism phase primarily involves improved scavenging of the reactive metabolite NAPQI due to accelerated GSH synthesis
5 Scavenging of the reactive metabolite NAPQI and decreasing of protein binding during the early phase occurs through increasing levels of GSH
6 Provision of increased amounts of cysteine to allow regeneration of GSH well beyond clearance of APAP, allowing for hepatocyte regeneration

Abbreviations: JNK, c-Jun-N-terminal kinase; GD, glutamate dehydrogenase; GSH, glutathione; NAC, N-acetylcysteine; HO-1, heme oxygenase-1; NAPQI, N-acetyl-para-benzo-quinone imine; Nrf2, nuclear factor erythroid 2-related factor 2.