Full Length Research Paper

Nrf2 transcription factor gene regulates basal transcription of mitochondrial superoxide dismutase enzyme in mouse brain

Muhammad Yalwa Gwarzo

Department of Chemical Pathology, Faculty of Medicine, Bayero University, Kano P. M. B. 3011 Kano, Nigeria. E-mail: mygwazo@yahoo.co.uk. Tel.:+2348067063239.

Accepted 9 July, 2009

   Abstract

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 .

Key words: Nuclear factor-erythroid 2-related factor-2 (Nrf2), antioxidant response element (ARE), mitochondrial superoxide dismutase (SOD2), Nrf2 mutant mice, chemopreventive agents.