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Maternal and Fetal Alpha‐Tocopherol Metabolites and Xenobiotic Metabolism Pathways in Sheep
Author(s) -
Granum Liana K,
Crimp Caitlin A,
Leonard Scott W,
Kutzler Michelle A,
Traber Maret G,
Mustacich Debbie J
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.996.21
Subject(s) - fetus , placenta , medicine , endocrinology , vitamin e , biology , metabolism , chemistry , pregnancy , biochemistry , antioxidant , genetics
The mechanism by which vitamin E (VE) may improve neonate outcomes is undetermined. Studies of maternal and fetal plasma VE suggest VE may not cross the placenta efficiently and the ability of the fetus to metabolize VE to CEHC (VE metabolic product) has not been determined. Therefore, VE, CEHC and the expression of proteins involved in VE metabolism, cytochrome P450 (CYP) 3A and 4F enzymes, were assessed in pregnant ewes, placentas and near‐term fetuses. VE in ewe liver (15.3 nmol/g) and kidney (11.8 nmol/g) were 3‐fold higher than in those in the fetus (4.4 and 3.6 nmol/g, respectively). Ewe plasma VE (2.9 μM) was 6‐fold fetal plasma VE (0.5 μM), while ewe plasma CEHC (2.9 nmol/ml) was double fetal plasma CEHC (1.3 nmol/ml). In contrast, fetal liver CEHC levels were elevated compared to ewe liver CEHC. Fetal amniotic and urine CEHC levels (4.2 and 13.8 nmol/ml, respectively) were 3‐ and 10‐fold fetal plasma CEHC levels. CYP4F enzymes were expressed in ewe liver, placenta and fetal liver, while CYP3A enzymes were expressed in ewe and fetal liver, but not placenta. These data are the first to suggest that the fetus and/or placenta are able to metabolize VE.