Biotin deficiency per se is teratogenic in mice.
We examined whether maternal biotin deficiency would potentiate the latent teratogenicity of relatively low doses of vitamin A in mice. The incidence and the type of gross congenital malformations (cleft palate, micrognathia, and micromelia) induced by biotin deficiency were similar among the groups given three different concentrations of vitamin A (4000, 12,000 and 60,000 IU) in the diet. Also, the type of these malformations was different from those (exencephaly, cleft palate and macroglossia) induced by a known teratogenic dose of vitamin A (1,200,000 IU). We conclude that in mice concentrations of vitamin A in the range of 4-10 times the level recommended by the National Research Council and biotin deficiency do not interfere with one another; also, biotin deficiency per se is teratogenic in mice.
Watanabe
T
T
Department of Hygiene and Preventive Medicine, Yamagata University School of Medicine, Japan.
Endo
A
A
D000014:Abnormalities, Drug-Induced; D000015:Abnormalities, Multiple / Q000209:etiology; D000818:Animals; D001710:Biotin / Q000172:deficiency*; D002972:Cleft Palate / Q000209:etiology; D000013:Congenital Abnormalities / Q000209:etiology*; D005260:Female; D007569:Jaw Abnormalities / Q000209:etiology; D017880:Limb Deformities, Congenital; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D011247:Pregnancy; D011248:Pregnancy Complications; D014801:Vitamin A / Q000008:administration & dosage / Q000633:toxicity*
D014801:Vitamin A; D001710:Biotin