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Feeding young adult mice high levels of dietary vitamin E (all-rac- α -tocopheryl acetate at 750 or 7,500 mg/kg) could not replace the protection by Gpx1 against the paraquat-induced lethality [70], although hepatic Gpx activities were elevated by ~40% in the Gpx1 −/− mice and by 17~24% the wild-type mice compared with those fed 0 or 75 mg of all-rac- α -tocopheryl acetate Contrary to the chick results, hepatic Gpx4 activities in both Gpx1 −/− and wild-type mice showed dose-dependent increases (36 and 48%, respectively) in response to the increases in dietary vitamin E supplementation