The results shown by the present study strongly suggest that NAC administration inhibited ethanol-induced oxidative stress (GSSG/GSH ratio) activating the Nrf2-ARE system, which is in line with a report that an analog of NAC, NACA, attenuated the oxidative stress induced by a traumatic brain injury in rats via the same antioxidant system (Zhou et al., 2018). This evidence concerns the gene NACA and injury.