Drug-Induced Liver Injury: Clinical Evidence of N-Acetyl Cysteine Protective Effects

Figure 2

Proposed molecular mechanism by which N-acetyl cysteine (NAC) ameliorates acute liver injury by targeting oxidative stress. Briefly, NAC can enhance the endogenous GSH levels to elicit antioxidant responses, mainly via Nrf2 activation and its linked antioxidant-detoxifying enzymes like SOD, GPx, GST, HO-1, and NQO1, to protecting against APAP-induced hepatotoxicity. Abbreviations: APAP: paracetamol/acetaminophen; NAPQI: N-acetyl-p-benzo-quinone imine; GSH: reduced glutathione; GSSH: oxidized glutathione; Nrf2: nuclear factor erythroid 2-related factor 2; Keap1: Kelch-like ECH-associated protein 1; CAT: catalase; SOD: superoxide dismutase; GPx: glutathione peroxidase; GST: glutathione s-transferase; HO-1: heme oxigenase-1; NQO1: oxidoreductase 1.