Vacca L, Hutchings D E
Dev Psychobiol. 1977 Mar;10(2):171-6. doi: 10.1002/dev.420100210.
Pregnant rats were administered a teratogenic dose of vitamin A excess on Days 17 and 18 of gestation and intubation controls received the vehicle alone. Pups were sacrificed at birth or on postnatal Days 5 or 10; the cerebellum was removed, frozen, and fixed in preparation for immunohistochemical localization of the brain specific protein, S-100. Vitamin A produced a transient delay in the appearance of S-100 in the external granular layer which was no longer evident on Days 5 and 10. These findings corroborate autoradiographic evidence that vitamin A temporarily interferes with neurogenesis. However, the early damage results in permanent behavioral deficits in adulthood despite apparent cytochemical repair.
在妊娠第17天和第18天，给怀孕大鼠给予致畸剂量的过量维生素A，经插管的对照组仅接受赋形剂。幼崽在出生时或出生后第5天或第10天被处死；取出小脑，冷冻并固定，以准备对脑特异性蛋白S-100进行免疫组织化学定位。维生素A导致外颗粒层中S-100的出现暂时延迟，在第5天和第10天不再明显。这些发现证实了放射自显影证据，即维生素A暂时干扰神经发生。然而，尽管有明显的细胞化学修复，但早期损伤会导致成年期永久性行为缺陷。
