Genetic or pharmacologic activation of Nrf2 signaling fails to protect against aflatoxin genotoxicity in hypersensitive GSTA3 knockout mice.

@article{Kensler2014GeneticOP,
  title={Genetic or pharmacologic activation of Nrf2 signaling fails to protect against aflatoxin genotoxicity in hypersensitive GSTA3 knockout mice.},
  author={Kevin H. Kensler and Stephen L. Slocum and Dionysios V Chartoumpekis and Patrick M. Dolan and Natalie M. Johnson and Zoran Ilic and Dana R. Crawford and Stewart Sell and John D. Groopman and Thomas Wells Kensler and Patricia A. Egner},
  journal={Toxicological sciences : an official journal of the Society of Toxicology},
  year={2014},
  volume={139 2},
  pages={293-300}
}
Mice are resistant to aflatoxin hepatotoxicity, primarily due to high expression of glutathione S-transferases (GSTs), and in particular the GSTA3 subunit. Nuclear factor erythroid 2 related factor 2 (Nrf2) signaling, which controls a broad-based cytoprotective response, was activated either genetically or pharmacologically in an attempt to rescue GSTA3 knockout mice from aflatoxin genotoxicity. Genetic activation of Nrf2 signaling was attained in a GSTA3: hepatocyte-specific Keap1 double… CONTINUE READING