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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., Whether an activation of xCT transporter function due to an increased substrate availability and/or an increased xCT expression plays a role in the NAC-induced reduction of hippocampal GSSG/GSH ratio, the administration of the xCT inhibitor SZ was expected to reduce or block such an effect of NAC

ME-3 consumption leads to an increase of the reduced/oxidized glutathione ratio in the body, and to an overall improvement of oxidative status

Wang YM, Gong FC, Qi X, Zheng YJ, Zheng XT, Chen Y, et al

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