The bioactivity of glucosinolates (GSs), and more specifically their hydrolysis products (GSHPs), has been well documented. These secondary metabolites evolved in the order Brassicales as plant defense compounds with proven ability to deter or impede the growth of several biotic challenges including insect infestation, fungal and bacterial infection, and competition from other plants. However, the bioactivity of GSHPs is not limited to activity that inhibits these kingdoms of life. Many of these compounds have been shown to have bioactivity in mammalian systems as well, with epidemiological links to cancer chemoprevention in humans supported by in vitro, in vivo, and small clinical studies. Although other chemopreventive mechanisms have been identified, the primary mechanism believed to be responsible for the observed chemoprevention from GSHPs is the induction of antioxidant enzymes, such as NAD(P)H quinone reductase (NQO1), heme oxygenase 1 (HO-1), glutamate-cysteine ligase catalytic subunit (GCLC), and glutathione S transferases (GSTs), through the Keap1-Nrf2-ARE signaling pathway. Induction of this pathway is generally associated with aliphatic isothiocyanate GSHPs, although some indole-derived GSHPs have also been associated with induction of one or more of these enzymes.
Keywords: Brassica; Nrf2; antioxidant enzymes; cancer; chemoprevention; detoxification; glucosinolate; hydrolysis product; phase II; quinone reductase.