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Teratogenicity of vitamin B6 deficiency: omphalocele, skeletal and neural defects, and splenic hypoplasia.

Abstract
Vitamin B(6) deficiency was induced in pregnant rats with a deficient diet and with 4-deoxypyridoxine, a B(6) antagonist. Treated animals developed typical skin changes of B(6) deficiency. Fetuses were small and appeared anemic. Major fetal malformations were omphalocele, exencephaly, cleft palate, micrognathia, digital defects, and splenic hypoplasia. This teratologic system was developed as a model for human syndromes that exhibit combined immunologic and neurologic or skeletal defects.
AuthorsS D Davis, T Nelson, T H Shepard
JournalScience (New York, N.Y.) (Science) Vol. 169 Issue 3952 Pg. 1329-30 (Sep 25 1970) ISSN: 0036-8075 [Print] United States
PMID5454144 (Publication Type: Journal Article)
Chemical References
  • Pyridines
  • Pyridoxine
  • Methanol
Topics
  • Animals
  • Brain (abnormalities)
  • Cleft Palate (etiology)
  • Disease Models, Animal
  • Female
  • Hernia, Ventral (etiology)
  • Limb Deformities, Congenital
  • Methanol
  • Micrognathism (etiology)
  • Organ Size
  • Pregnancy
  • Pregnancy Complications
  • Pyridines
  • Pyridoxine (antagonists & inhibitors)
  • Rats
  • Spleen (abnormalities)
  • Vitamin B 6 Deficiency (chemically induced, complications)

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