The isoflavones equol and genistein do not induce xenobiotic-metabolizing enzymes in mouse and in human cells

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Abstract
1. In view of the anticarcinogenic effects of the isoflavonoid genistein and the known ability of various flavonoids to induce carcinogen-metabolizing enzymes, the ability of the isoflavonoids genistein and equol to induce these enzymes was studied in mouse. 2. In comparison with induction by the positive control beta -naphthoflavone (40 mg kg i.p.4days)neither genisteinorequol(0 4-40 mg kg i.p.4 days) gave asignificant induction of ethoxyresorufin O -deethylase, p -nitrophenol oxidase or immunoreactive CYP1A2 or CYP2E1. There was also no induction of erythromycin- N -demethylase or elevation of immunoreactive CYP3A1. 3. In contrast with the induction by beta -naphthoflavone of glutathione S -transferase protein and activity towards 1-chloro-2,4-dinitrobenzene, neither isoflavone exhibited such induction. 4. Response elements for human CYP1A1, glutathione S -transferase lambda a and the xenobioticresponse element (XRE) in HepG2cells wereactivatedby beta -naphthoflavone but not by genistein or equol. 5. The isoflavones have been found not to induce a range of enzymes involved in carcinogen metabolism. The lack of enzyme induction differs from the characteristics of many other flavonoids. The results do not support the monofunctional induction of GST as a basis of anticarcinogenicity.