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BIOTIN INFLUENCES PALATAL DEVELOPMENT OF MOUSE EMBRYOS IN ORGAN-CULTURE
被引:36
作者:
WATANABE, T
DAKSHINAMURTI, K
PERSAUD, TVN
机构:
[1] UNIV MANITOBA, FAC MED, DEPT BIOCHEM & MOLEC BIOL, WINNIPEG, MB R3E 0W3, CANADA
[2] UNIV MANITOBA, FAC MED, DEPT ANAT, WINNIPEG, MB R3E 0W3, CANADA
关键词:
BIOTIN DEFICIENCY;
PALATAL DEVELOPMENT;
ORGAN CULTURE;
TERATOGENICITY;
MICE;
D O I:
10.1093/jn/125.8.2114
中图分类号:
R15 [营养卫生、食品卫生];
TS201 [基础科学];
学科分类号:
100403 ;
摘要:
Maternal biotin deficiency is strongly teratogenic in CD-1 mice. The most common malformations are craniofacial and limb defects such as cleft palate, micrognathia and micromelia. The effect of biotin deficiency on palatal development in mouse embryos on d 12 of gestation was studied by culturing mouse embryonic palates in serum-free medium using a suspension culture system. In control embryos palatal processes developed to the fused stage after 72 h in culture. The fusion of palatal processes was further increased by the addition of biotin (10(-8) mol/L) to the medium. The addition of organic acids such as propionic, beta-methyl crotonic or beta-hydroxy isovaleric acids as well as avidin to the medium did not affect the stage of palatal formation. Cycloheximide completely blocked the fusion of palatal shelves. In embryos from biotin-deficient mice, the incidence of fusion between the palatal shelves was <7% and increased to >30% when biotin (10(-8)-10(-6) mol/L) was added to the medium. The addition of fatty acids to the organ culture medium did not have any effect on the fusion of palatal processes. The incorporation of S-35-methionine into protein from biotin-deficient embryo explants was 88% of that in controls. The results indicate that biotin deficiency may interfere directly with synthesis of specific proteins and the formation of palatal processes.
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页码:2114 / 2121
页数:8
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