![]() |
|
|
Department of Hygiene and Preventive Medicine, Yamagata University School of Medicine, Yamagata, 990-23, Japan
The teratogenicity of maternal biotin deficiency of mice, rats and Syrian hamsters was compared. Biotin deficiency during pregnancy caused severe malformations and growth retardation in mouse fetuses. The malformations were mainly cleft palate, micrognathia, micromelia and open eyelid. The ICR and C57BL strains of mice were more susceptible than the A/Jax strain to biotin deficiency. In rats, no malformations were seen in the fetuses from biotin-deficient dams. In hamsters, embryonic lethality was very high in biotin-deficient dams, and teratogenicity of biotin deficiency was rather equivocal. The results of measurements of the maternal and fetal biotin content suggest that a possible underlying mechanism is a difference in the efficiency of the mother-to-fetus transport of biotin among these species.
KEY WORDS: biotin deficiency teratogenicity mice rats Syrian hamsters strain difference species difference
1 To whom correspondence should be addressed.
Manuscript received 7 December 1987. Revision accepted 28 September 1988.
This article has been cited by other articles:
![]() |
R. Takechi, A. Taniguchi, S. Ebara, T. Fukui, and T. Watanabe Biotin Deficiency Affects the Proliferation of Human Embryonic Palatal Mesenchymal Cells in Culture J. Nutr., April 1, 2008; 138(4): 680 - 684. [Abstract] [Full Text] [PDF] |
||||