GSTT1 genotype modifies the association between cruciferous vegetable intake and the risk of myocardial infarction
GSTT1 genotype modifies the association between cruciferous vegetable intake and the risk of myocardial infarction
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DOI:
10.1093/ajcn/86.3.752
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发表时间:
2007-09-01
影响因子:
7.1
通讯作者:
Campos, Hannia
中科院分区:
文献类型:
--
作者:
Cornelis, Marilyn C.;El-Sohemy, Ahmed;Campos, Hannia
Background: Cruciferous vegetables are a major dietary source of isothiocyanates that may protect against coronary heart disease. Isothiocyanates induce glutathione S-transferases (GSTs), polymorphic genes that code for enzymes that conjugate isothiocyanates, as well as mutagens and reactive oxygen species, to make them more readily excretable.Objective: The objective of the study was to determine whether GST genotypes modify the association between cruciferous vegetable intake and the risk of myocardial infarction (MI).Design: Cases (n = 2042) with a first acute nonfatal MI and population-based controls (n = 2042) living in Costa Rica, who were matched for age, sex, and area of residence, were genotyped for a deletion polymorphism in GSTM1 and GSTT1 and an Ile105Val substitution in GSTP1. Cruciferous vegetable intake and smoking status were determined by questionnaire. Odds ratios (ORs) and 95% Cls for MI were estimated by unconditional logistic regression.Results: Compared with the lowest tertile of cruciferous vegetable intake, the highest tertile was associated with a lower risk of MI among persons with the functional GSTT1 *1 allele (OR: 0.70; 95% Cl: 0.58, 0.84) but not among those with the GSTT1*0*0 genotype (OR: 1.23; 95% Cl: 0.83, 1.82) (P = 0.006 for interaction). This protective effect among those with the GSTT1*1 allele was greater for current smokers (OR: 0.54; 95% Cl: 0.36, 0.79) than for nonsmokers. GSTP1 and GSTM1 did not modify the association between cruciferous vegetable intake and MI.Conclusions: Consumption of cruciferous vegetables was associated with a lower risk of MI among those with a functional GSTT1*1 allele, which suggests that compounds that are detoxified by this enzyme contribute to the risk of MI.