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. Author manuscript; available in PMC: 2009 Apr 15.
Published in final edited form as: Free Radic Biol Med. 2008 Jan 31;44(8):1617–1623. doi: 10.1016/j.freeradbiomed.2008.01.016

Figure 5.

Figure 5

Greatly simplified scheme of postulated function of the Nrf2-antioxidant response element (ARE) system in combating oxidative stress. Under basal conditions, endogenous ROS (reactive oxygen species) cause release (1) of Nrf2 from Keap1 and (2) Nrf2 enters the nucleus (broken-line circle) and binds to AREs in the promoter regions of genes of some antioxidant enzymes. As a result of the Nrf2-ARE interaction, (3) antioxidant enzymes are produced, (4) reducing the concentrations and effects of ROS and lessening the effect of ROS on Keap1 binding of Nrf2.

Selenium deficiency decreases the antioxidant selenoproteins, allowing the ROS to increase and activate the Nrf2-ARE system. Antioxidant enzymes that are not selenoproteins are induced until the ROS are brought into balance at a higher concentration that maintains the activation of the Nrf2-ARE system.