Evidence suggests that the Nrf2 transcription factor participates in the regulation of expression of genes that contain functional antioxidant responsive elements (AREs) in their promoter regions. Previous studies have shown that induction of glutathione-S- transferases (GST) and NADPH quinone reductase 1 (NQO1) by t-butylated hydroxy anisole (BHA) is impaired in the livers of Nrf2(-/-) mice. Basal expression of certain antioxidant enzymes is also lower in the livers of Nrf2 (-/-) mice. Results indicate that Nrf2 contributes to basal expression but not inducible expression of mitochondrial superoxide
dismutase. SOD2 level was affected in the Nrf2(-/-) and about 2-fold lower than the Nrf2(+/+) mouse control. The dietary additives caused a small induction of SOD2 in the Nrf2(-/-) mouse brain, ethoxyquin and
kahwoel palmitate each induced SOD2 marginally, while oltipraz and indole-3-carbinol caused 1.5 fold induction in the Nrf2(-/-) mouse brain. In contrast, there was no obvious effect on SOD2 in the Nrf2(+/+) mouse brain by any of the chemicals used .