Abstract
Estrogen exposure plays a role in breast cancer (BC) development. A novel estrogen biomarker, the estrogen DNA adduct (EDA) ratio, was shown to be elevated in women at high-risk of BC and among BC cases. Modifiable factors may impact the EDA ratio, with studies demonstrating that resveratrol reduces EDA ratio in vitro. We sought to examine the hypothesis that dietary intake of fruits and vegetables is inversely associated with EDA ratio. This analysis was conducted in 53 pre-menopausal, healthy women aged 40-45 years from a cross-sectional study in which participants provided first-void urine samples and 3-day food records. Urine samples were analyzed using ultraperformance liquid chromatography/tandem mass spectrometry. The EDA ratio was calculated as the estrogen-DNA adducts divided by estrogen metabolites and conjugates. A trend test was used to assess associations between tertiles of dietary intake using linear regression. After adjustment for age, total energy, percent adiposity, serum estradiol and estrone-sulfate, we observed inverse associations of EDA ratio with carbohydrate consumption (P=0.01) and vegetable intake (P =0.01). EDA ratio was inversely associated with 5 botanical groups (Chenopodiaceae: P=0.02; Umbelliferae: P=0.03; Compositae: P=0.01; Ericaceae: P=0.01; Musaceae: P=0.03) but not fruit intake overall. Although these data require replication before conclusions are drawn, this report suggests an inverse association between vegetable and carbohydrate consumption and EDA ratio. While more information is still needed, these findings suggest a link between dietary intake and a biomarker that is both associated with high-risk BC status and associated with modifiable factors.
Highlights
Estrogen exposure has been implicated in breast cancer (BC) development [1]
An elevated estrogen DNA adduct (EDA) ratio was associated with low total carbohydrate consumption (P = 0.01), low vegetable intake (P = 0.01), low fruit and vegetable intake (P = 0.03), high fish and shellfish consumption (P = 0.03), and high egg consumption (P = 0.03) after adjustment for age, total energy intake, percent adiposity, serum E2 and E1S (Table 2)
Based on these findings [i.e., opposite directions in the associations for botanical groupings and protein-based groups], we further examined the association between the percent of energy consumed from macronutrients
Summary
Estrogen exposure has been implicated in breast cancer (BC) development [1]. While much of the focus has been upon estrogen’s proliferative effects, more recently research has focused on estrogen’s genotoxic effects [2] [3]. Greater adduct formation with the 4-CE compared to the 2CE has been observed, likely as a result of the location of the hydroxy group [6] Within this pathway, enzymes are involved in both activating and inactivating CE metabolites [3] [10]. CYP1A1 and CYP1B1 convert E1/E2 to the 2- and 4-CE, respectively; while Phase II enzymes, including catechol-O-methyltransferase (COMT), glutathione S transferase (GST), UDP-glucuronosyltransferase (UGT), sulfotransferase (SULT), and NADPH-quinone reductase (NQ01), can inactivate CEs. there is biological plausibility for a role of EDAs in BC development as well as indication that this pathway involves a number of enzymes. Results: After adjustment for age, total energy, percent adiposity, serum estradiol and estrone-sulfate, we observed inverse associations of EDA ratio with carbohydrate consumption (P = 0.01) and vegetable intake (P = 0.01).
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