Elsevier

The Journal of Nutrition

Volume 132, Issue 10, October 2002, Pages 2991-2994
The Journal of Nutrition

Brassica, Biotransformation and Cancer Risk: Genetic Polymorphisms Alter the Preventive Effects of Cruciferous Vegetables1

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The chemoprotective effect of cruciferous vegetables is due to their high glucosinolate content and the capacity of glucosinolate metabolites, such as isothiocyanates (ITC) and indoles, to modulate biotransformation enzyme systems (e.g., cytochromes P450 and conjugating enzymes). Data from molecular epidemiologic studies suggest that genetic and associated functional variations in biotransformation enzymes, particularly glutathione S-transferase (GST)M1 and GSTT1, which metabolize ITC, alter cancer risk in response to cruciferous vegetable exposure. Moreover, genetic polymorphisms in receptors and transcription factors that interact with these compounds may further contribute to variation in response to cruciferous vegetable intake. This review outlines the metabolism and mechanisms of action of cruciferous vegetable constituents, discusses the recent human studies testing effects of cruciferous vegetables on biotransformation systems and summarizes the epidemiologic and experimental evidence for an effect of genetic polymorphisms in these enzymes on response to cruciferous vegetable intake. Taken together, genetic differences in biotransformation enzymes and the factors that regulate them, as well as variation in glucosinolate content of cruciferous vegetables and the methods used to prepare these foods underscore the multiple layers of complexity that affect the study of gene-diet interactions and cancer risk in humans.

Key words:

isothiocyanates
cruciferae
biotransformation
polymorphism
chemoprevention

Abbreviations:

AhR
aryl hydrocarbon receptor
ARE/EpRE;
antioxidant/electrophile response element
DIM
diindolylmethane
GST
glutathione S-transferase
I3C
indole-3-carbinol
ITC
isothiocyanate
NQO1
NAD(P)H:quinone oxidoreductase
PEITC
phenethyl ITC
UGT
UDP-glucuronosyltransferase
XRE
xenobiotic response element

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1

The work in this article that was performed in J.W.L.’s laboratory was supported by National Institutes of Health Grant R01 CA70913 and S.P. is supported by National Cancer Institute Training grant CA80416.