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.[1]References
- Biotin deficiency per se is teratogenic in mice. Watanabe, T., Endo, A. J. Nutr. (1991) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
