Smith C J, Kelleher P C
Teratology. 1977 Aug;16(1):71-8. doi: 10.1002/tera.1420160112.
Alpha-fetoprotein and albumin were quantified in the sera and amniotic fluids from control, Vitamin A-treated non-exencephalic and Vitamin A-treated exencephalic rat fetuses. Exencephaly was associated with amniotic fluid alpha-fetoprotein concentrations which were significantly elevated over those of Vitamin A-treated non-exencephalic and of untreated fetuses. Amniotic fluid albumin concentrations also were higher in the exencephalic fetuses than in the non-exencephalic fetuses. Serum alpha-fetoprotein and albumin concentrations were lower in the exencephalic than in the non-exencephalic fetuses. The results are cosistent with simple diffusion across a defective barrier as the cause of elevated amniotic fluid alpha-fetoprotein concentrations in the presence of open neural tube defects. This experimental model of neural tube defects result in changes in amniotic fluid alpha-fetoprotein similar to those changes found in human amniotic fluid alpha-fetoprotein concentrations in the presence of neural tube defects.
对对照组、维生素A处理的无脑儿和维生素A处理的脑膨出大鼠胎儿的血清和羊水进行甲胎蛋白和白蛋白定量分析。脑膨出与羊水中甲胎蛋白浓度有关,该浓度比维生素A处理的无脑儿和未处理胎儿的浓度显著升高。脑膨出胎儿的羊水白蛋白浓度也高于无脑儿胎儿。脑膨出胎儿的血清甲胎蛋白和白蛋白浓度低于无脑儿胎儿。这些结果与在开放性神经管缺陷存在时,通过有缺陷的屏障进行简单扩散导致羊水甲胎蛋白浓度升高的情况一致。这种神经管缺陷的实验模型导致羊水中甲胎蛋白的变化,类似于在神经管缺陷存在时人类羊水中甲胎蛋白浓度的变化。