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In hepatic phase II detoxification, glutathione conjugation (catalysed by glutathione S-transferases) is one of the principal mechanisms by which the liver neutralises and prepares toxins, drug metabolites and environmental pollutants for excretion.⁴ NAC — which delivers cysteine intracellularly — is the established treatment of choice for acetaminophen toxicity in dogs, precisely because it replenishes the cysteine needed for emergency glutathione synthesis when hepatic stores are acutely depleted.⁴ Beyond emergency toxicology, a study in beagle dogs with experimentally induced obstructive jaundice demonstrated that NAC administration increased both serum and hepatic glutathione concentrations as well as hepatic ATP levels, suggesting support for both antioxidant capacity and mitochondrial energy metabolism in the compromised liver.⁷ Research in canine diabetes models has shown that NAC combined with insulin exerted protective effects against liver injury by inhibiting the NLRP3/NF-κB inflammatory pathway, reducing hepatocyte pyroptosis (inflammatory cell death) and improving liver function enzyme profiles.⁸ While these were experimental disease models, the mechanisms are relevant to the broader hepatoprotective potential of maintaining adequate cysteine status

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