期刊
TOXICOLOGY AND APPLIED PHARMACOLOGY
卷 306, 期 -, 页码 79-85出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.taap.2016.07.007
关键词
Cadmium; Neural tube defects; Fetal growth restriction; Folate; Placenta; Proton-coupled folate transporter
资金
- National Natural Science Foundation of China [81473016, 81172711]
- Key Projects of outstanding Youth Talent Support Program in Anhui Provincial University [gxyqZD2016056]
- Grants for Scientific Research of BSKY [XJ201522]
- Top-notch Youth Talent Support Program from Anhui Medical University
Previous studies found that maternal Cd exposure on gestational day (GD)9 caused forelimb ectrodactyly and tail deformity, the characteristic malformations. The aim of the present study was to investigate whether maternal Cd exposure on GD8 induces fetal neural tube defects (NTDs). Pregnant mice were intraperitoneally injected with CdCl2 (2.5 or 5.0 mg/kg) on GD8. Neither forelimb ectrodactyly nor tail deformity was observed in mice injected with CdCl2 on GD8. Instead, maternal Cd exposure on GD8 resulted in the incidence of NTDs. Moreover, maternal Cd exposure on GD8 resulted in fetal growth restriction. In addition, maternal Cd exposure on GD8 reduced placental weight and diameter. The internal space of maternal and fetal blood vessels in the labyrinth layer was decreased in the placentas of mice treated with CdCl2. Additional experiment showed that placental PCFT protein and mRNA, a critical folate transporter, was persistently decreased when dams were injected with CdCl2 on GD8. Correspondingly, embryonic folate content was markedly decreased in mice injected with CdCl2 on GD8, whereas Cd had little effect on folate content in maternal serum. Taken together, these results suggest that maternal Cd exposure during organogenesis disturbs transport of folate from maternal circulation to the fetuses through down-regulating placental folate transporters. (C) 2016 Elsevier Inc. All rights reserved.
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