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Vol. 56, Issue 4, 760-767, October 1999
Cellular Defense and Carcinogenesis Section, Basic Research
Laboratory, Division of Basic Sciences, National Cancer Institute,
Frederick Cancer Research and Development Center, National Institutes
of Health, Frederick, Maryland
We investigated the effect of resveratrol, a constituent of the
human diet that has been shown to inhibit aryl hydrocarbon-induced carcinogenesis in animals, on the carcinogen activation pathway regulated by the aryl hydrocarbon receptor. Resveratrol inhibited the
metabolism of the environmental aryl hydrocarbon
benzo[a]pyrene (B[a]P) catalyzed by microsomes
isolated from B[a]P-treated human hepatoma HepG2 cells. Resveratrol
competitively inhibited, in a concentration-dependent manner, the
activity of the carcinogen activating enzymes cytochrome P-450
(CYP)1A1/CYP1A2 in microsomes and intact HepG2 cells. Resveratrol
inhibited the B[a]P-induced expression of the CYP1A1
gene, as measured at the mRNA and transcriptional levels. Resveratrol
abolished the binding of B[a]P-activated nuclear aryl hydrocarbon
receptor to the xenobiotic-responsive element of the
CYP1A1 promoter but did not itself bind to the receptor. Resveratrol was also effective in inhibiting CYP1A1
transcription induced by the aryl hydrocarbon
dimethylbenz[a]anthracene in human mammary carcinoma
MCF-7 cells. These data demonstrate that resveratrol inhibits aryl
hydrocarbon-induced CYP1A activity in vitro by directly inhibiting
CYP1A1/1A2 enzyme activity and by inhibiting the signal transduction
pathway that up-regulates the expression of carcinogen activating
enzymes. These activities may be an important part of the
chemopreventive activity of resveratrol in vivo.
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