期刊
DEVELOPMENTAL DYNAMICS
卷 231, 期 1, 页码 221-231出版社
WILEY
DOI: 10.1002/dvdy.20107
关键词
neural tube defect; craniofacial; neural crest; folic acid; folinic acid; Metafolin
资金
- NHLBI NIH HHS [HL66398] Funding Source: Medline
- NICHD NIH HHS [HD39195, HD39081] Funding Source: Medline
- NIDCR NIH HHS [DE13616] Funding Source: Medline
- NIEHS NIH HHS [ES09106, ES04917] Funding Source: Medline
Inactivation of folate binding protein-1 (Folbp1) adversely impacts murine embryonic development, as nullizygous embryos (Folbp1(-/-)) die in utero. Administration of folinic acid (N5-formyl-tetrahydrofolate) to Folbp1-deficient dams before and throughout gestation rescues the majority of embryos from premature death; however, a portion of surviving embryos develop structural malformations, including neural tube defects. We examined whether maternal supplementation with L-N5-methyl-tetrahydrofolate (L-5M-THF) has superior protective effects on embryonic development of Folbp1(-/-) fetuses compared with L-N5-formyl-tetrahydrofolate (L-5F-THF). We also examined the critical period during gestation when folate supplementation is most beneficial to the developing Folbp1(-/-) embryos. Folbp1(-/-) pups presented with a range of malformations involving the neural tube, craniofacies, eyes, and abdominal wall. The frequencies of these malformations decreased with increasing folate dose, regardless of the form used. There was no additional benefit provided by L-5M-THF compared with L-5F-THF. Despite rescuing the phenotype in Folbp1(-/-) embryos, no significant elevation of Folbp1(-/-) maternal folate levels was observed with supplementation. (C) 2004 Wiley-Liss, Inc.
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