Studies of the etiology of thalidomide dysmorphogenesis.
Studies of the etiology of thalidomide dysmorphogenesis.
复制标题
沙利度胺畸形发生的病因学研究。
DOI：
10.1002/tera.1420140110
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发表时间：
1976
期刊：
影响因子：
--
通讯作者：
W. Mcbride
中科院分区：
文献类型：
--
作者：
W. Mcbride
在妊娠第8-12天给药沙利度胺，剂量为150 ~ 250 mg/kg/天。这些雌性生育了40个后代，其中21个是畸形的。四只对照雌性产下34只后代，没有一只是畸形的。电镜观察13、15、17、21天对照和实验胚胎及胎儿的C6、C7神经节。在13天的实验胚胎中，背根神经节的神经元和轴突发生了退行性改变，即至少比在兔子中报道的最早的沙利度胺障碍症状早16小时（Vickers, 1967）。由于兔背根神经节在第11天和第12天形成，第13天的明显变化表明神经元和轴突的变性可能是沙利度胺诱导的外周畸形的一个致病因素。
Thalidomide was administered to pregnant rabbits in dosages of 150-250 mg/kg/day on days 8-12 of gestation. These females produced 40 offspring, 21 of which were deformed. Four control females produced 34 offspring, none of which was deformed. The C6 and C7 ganglia of day-13, -15, -17, and -21 control and experimental embryos and fetuses were examined electron microscopically. Degenerative changes were found in the neurons and axons of dorsal root ganglia in day-13 experimental embryos, i.e., at least 16h before the earliest signs of thalidomide dysmelia have been reported in rabbits (Vickers, '67). Since the dorsal root ganglia form in rabbits on days 11 and 12 the changes evident at day 13 indicate that degeneration of neurons and axons may be a pathogenetic factor in thalidomide-induced peripheral deformities.