Love A M, Vickers T H
Br J Exp Pathol. 1971 Dec;52(6):656-68.
Limb defects were induced in the offspring of rats by giving 200,000-800,000 i.u. per kg. vitamin A on days 10-16 of their pregnancy. The malformations were symmetrical and there was no fore or hind limb predominance but fore limb lesions tended to be more severe. As severity increased there was progressive distoproximal suppression of digital rays commencing with digits 1 and 5 then extending to digits 2 and 3. Digit 4 was affected last. Syndactyly of soft tissues and bone was a part of the process and could produce single composite digits. Deletion of digits occurred and could result from pure reduction defects or from syndactyly. The defect pattern and the sequence of digit involvement was fairly constant and matching patterns of reduction and fusion anomalies probably affected the carpal and the tarsal bones. Long bones showed varying degrees of shortening and deformity attributable to suppressed endochondral and periosteal bone formation. Repair phenomena following cessation of the treatment were in evidence. It is suggested that the skeletal malformations in the limbs result from first disturbed bone organogenesis and then from impeded postorganogenic bone growth.
在大鼠怀孕第10至16天，给其每千克体重注射200,000 - 800,000国际单位的维生素A，可导致其后代出现肢体缺陷。畸形是对称的，前肢和后肢没有明显的优势，但前肢病变往往更严重。随着严重程度的增加，从第1和第5指开始，数字射线逐渐向近端抑制，然后扩展到第2和第3指。第4指最后受到影响。软组织和骨骼的并指是这个过程的一部分，可能会产生单个复合指。指的缺失会发生，可能是由于单纯的发育不全缺陷或并指。缺陷模式和指受累的顺序相当恒定，减少和融合异常的匹配模式可能影响腕骨和跗骨。长骨显示出不同程度的缩短和畸形，这归因于软骨内和骨膜骨形成的抑制。治疗停止后的修复现象很明显。有人认为，肢体的骨骼畸形首先是由于骨器官发生紊乱，然后是由于器官发生后骨生长受阻。
