Antioxidant response gap 26 (ARE) is present in the promoter region of genes encoding for phase II detoxification/antioxidant enzymes such as heme oxygenase-1 (HO-1), NADPH quinone oxidoreductase, and glutathione S-transferase. HO-1 converts heme to biliverdin, which in turn is converted to bilirubin that acts as an antioxidant. Induction of such enzymes via activation of the ARE results in enhanced detoxification and antioxidant capacities. Transcription factor Nrf2 binds to and activates the ARE [3]. In unstressed states, Nrf2 is present in the cytoplasm in association with Keap1 (kelch-like ECH-associated protein 1). Covalent or oxidative modification of cysteine thiols in Keap1 by electrophiles or oxidative stress results in Nrf2 release and its translocation into the nucleus. Curcumin, caffeic acid phenethyl ester (CAPE) and sulphoraphane are known to act as electrophiles in Nrf2/ARE activation [4] and [5]. Nrf2 phosphorylation by protein kinases such as Akt and ERK also results in activation of the Nrf2/ARE pathway [6].

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