Increased vitamin E intake is associated with higher α-tocopherol concentration in the maternal circulation but higher α-carboxyethyl hydroxychroman concentration in the fetal circulation1,2,3

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Background: The transfer of vitamin E across the placenta is limited, but no data exist on the concentrations of vitamin E metabolites carboxyethyl hydroxychromans (α- and γ-CEHCs) in the fetal circulation.

Objective: We measured α- and γ-CEHC concentrations in maternal and umbilical cord blood pairs and examined their relations to circulating vitamin E (α- and γ-tocopherol) and maternal dietary vitamin E intake.

Design: Healthy, pregnant women were enrolled from Oregon Health and Science University’s obstetric clinic (<22 wk gestation), and at least one fasting blood sample and a previous day’s 24-h diet recall were collected during their pregnancy (n = 19). Umbilical cord blood samples were obtained at the time of delivery and were analyzed for α- and γ-tocopherol, α- and γ-CEHC, and total lipid concentrations.

Results: Mean (±SD) concentrations of umbilical cord blood α-CEHC (30.2 ± 28.9 nmol/L) and γ-CEHC (104.5 ± 61.3 nmol/L) were not significantly different from maternal concentrations (P = 0.07 and 0.08, respectively), but metabolite:tocopherol ratios were significantly higher in cord blood (P < 0.01 and 0.001, respectively). Maternal α-tocopherol:total lipids ratios were correlated with cord blood α-CEHCs (r = 0.67, P = 0.004), and higher vitamin E intakes were associated with higher cord blood α-CEHC concentrations (r = 0.75, P < 0.003).

Conclusion: Higher maternal intake of vitamin E during pregnancy may result in increased metabolite concentrations in the fetal circulation, suggesting increased maternal or fetal liver metabolism of vitamin E. This trial was registered at clinicaltrials.gov as NCT00632476.

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1

From the Graduate Programs in Human Nutrition (SD and MBG), the Department of Molecular and Medical Genetics (MBG), and the Department of Pediatrics (MDG and CTM), School of Medicine, Oregon Health and Science University, Portland, OR; and the Linus Pauling Institute, Oregon State University, Corvallis, OR (SWL and MGT).

2

Supported by NIH grant K23 NHLBI HL080231 and the Oregon Clinical and Translational Research Institute (OCTRI); grant no. ULI RR024140 from the National Center for Research Resources, a component of the NIH and the NIH Roadmap for Medical Research; and the Linus Pauling Institute.

3

Address correspondence to CT McEvoy, Department of Pediatrics, Mail Code CDRC-P, 3181 SW Sam Jackson Park Road, Oregon Health and Science University, Portland, OR 97239. E-mail: [email protected]