Vitamin B6 deficiency was induced in pregnant rats with a deficient diet and with 4-deoxypyridoxine, a B6 antagonist. Treated animals developed typical skin changes of B6 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.

Vitamin B6 deficiency in pregnant rats leads to fetal malformations, including omphalocele, exencephaly, cleft palate, and splenic hypoplasia.

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Teratogenicity of Vitamin B6 Deficiency: Omphalocele, Skeletal and Neural Defects, and Splenic Hypoplasia

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