Susceptibility to teratogenicity of hypervitaminosis-A in X-monosomy mice.
We previously showed that the incidence of external malformations induced by biotin deficiency did not differ either between XO and XX dams or between XO and XX fetuses. To clarify whether this phenomenon is specific to biotin deficiency or more generally associated with other teratogens, we examined whether XO mice are more susceptible to teratogenic effects of hypervitaminosis-A. Pregnant XO and XX mice were given an excessive vitamin A diets (1.0 to 1.5 x 10(6) IU/kg) from days 0 to 17 of gestation. Maternal hypervitaminosis-A produced a high incidence of external malformations (65 to 80%), skeletal anomalies (33 to 47%), and variations (99 to 100%) in the fetuses. However, there is no difference in their incidences between XO and XX dams or between XO and XX fetuses. Together with previous findings, this suggests that developmental stability of the mouse embryo is not affected by missing of one whole X chromosome even with exposure to teratogens.
Omoe
K
K
Department of Hygiene and Preventive Medicine, Yamagata University School of Medicine, Japan.
Endo
A
A
D000782:Aneuploidy; D000818:Animals; D002872:Chromosome Deletion; D003433:Crosses, Genetic; D005314:Embryonic and Fetal Development / Q000187:drug effects; D005260:Female; D006986:Hypervitaminosis A / Q000235:genetics*; D008297:Male; D051379:Mice; D008817:Mice, Mutant Strains; D011247:Pregnancy; D012098:Reproduction / Q000187:drug effects; D013723:Teratogens / Q000633:toxicity*; D014801:Vitamin A / Q000633:toxicity*; D014960:X Chromosome
D013723:Teratogens; D014801:Vitamin A