Watanabe T, Endo A
Department of Hygiene and Preventive Medicine, Yamagata University School of Medicine, Japan.
J Nutr. 1991 Jan;121(1):101-4. doi: 10.1093/jn/121.1.101.
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.
我们研究了母体生物素缺乏是否会增强相对低剂量维生素A对小鼠的潜在致畸性。在饮食中给予三种不同浓度维生素A（4000、12000和60000国际单位）的各组中，由生物素缺乏诱导的明显先天性畸形（腭裂、小颌畸形和短肢畸形）的发生率和类型相似。此外，这些畸形的类型与已知致畸剂量维生素A（1200000国际单位）诱导的畸形（无脑畸形、腭裂和巨舌症）不同。我们得出结论，在小鼠中，维生素A浓度在国家研究委员会推荐水平的4至10倍范围内，与生物素缺乏不会相互干扰；此外，生物素缺乏本身在小鼠中具有致畸性。
