High sensitivity of Nrf2 knockout mice to acetaminophen hepatotoxicity associated with decreased expression of ARE-regulated drug metabolizing enzymes and antioxidant genes.

By A. Enomoto, K. Itoh, Eiko Nagayoshi, Junko Haruta, Toyoe Kimura, T. O'connor, T. Harada, Masayuki Yamamoto. Toxicological Sciences, 2001

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Keap1 Is a Redox-Regulated Substrate Adaptor Protein for a Cul3-Dependent Ubiquitin Ligase Complex (2004, neutral): “sensitivity to chemical-induced stresses (4, 10, 13, 18), hyper-”
Identification of Nrf2-regulated genes induced by the chemopreventive agent sulforaphane by oligonucleotide microarray. (2002, background): “Lack of or low expression of all these glutathione-associated genes in nrf2-deficient mice undoubtedly makes them more susceptible to xenobiotic toxicities ( 12 , 14).”
Molecular mechanisms of the Keap1–Nrf2 pathway in stress response and cancer evolution (2011, background): “1997), but they are susceptible to various chemical and physical insults (Chan & Kan 1999; Enomoto et al. 2001; Yoh et al. 2001).”
The importance of antioxidants which play the role in cellular response against oxidative/nitrosative stress: current state (2015, background): “The function of Nrf2 and its downstream proteins has been shown to be important for protection against oxidative/nitrosative stress- or chemical-induced cellular damage in liver [48, 49] and lung [50] as well as for prevention of cancer formation in the gastrointestinal tract [51, 52] and promotion ”
Role of nrf2 in oxidative stress and toxicity. (2013, background): “At doses relatively nontoxic to wild-type mice, Nrf2 KO mice showed increased serum ALT enzyme activity, severe hepatocellular injury, and even death from liver failure (13, 125).”