Reiners J, Löfberg B, Kraft J C, Kochhar D M, Nau H
Institute of Toxicology and Embryopharmacology, Free University Berlin, F.R.G.
Reprod Toxicol. 1988;2(1):19-29. doi: 10.1016/s0890-6238(88)80005-4.
The transplacental pharmacokinetics of single teratogenic doses of etretinate and motretinide were compared with particular emphasis on distribution and concentrations in the exposed embryos of the free acid metabolite, etretin. The three aromatic retinoids were also tested for their direct inhibitory effect on chondrogenesis in the limb bud mesenchymal cell "micromass" culture assay. After a standard dose of 100 mg/kg administered on day 11 of gestation in NMRI mice, all three compounds were teratogenic, but they differed from each other in potency. Etretinate was most active as a teratogen, equalling the potency of our standard all-trans-retinoic acid; every exposed fetus was deformed with severe shortening of all limb bones as well as cleft palate. Etretin was less potent than etretinate, and motretinide was considerably less active as a teratogen than the other two. In the in vitro assay, only etretin suppressed chondrogenesis and this activity was equivalent to that of all-trans-retinoic acid (IC50 of 12 ng/ml). Both etretinate and motretinide (which contain an ethyl ester and ethylamide terminal group, respectively) were essentially inactive in vitro, demonstrating the fact that a free carboxylic group may be a requirement for the in vitro suppression of chondrogenesis. These differences between the results obtained in vivo and in vitro could be resolved by pharmacokinetic investigations using HPLC methods. Both etretinate and motretinide were metabolized in vivo to etretin, their likely common teratogenic metabolite. The high teratogenic potency of etretinate was probably the result of high concentrations as well as AUC values of its metabolite etretin in the embryo. On the other hand, the comparatively low teratogenicity of motretinide could be related to approximately 5 x lower embryonic peak levels as well as AUC values of etretin. A comparison of these results with those previously obtained for all-trans- and 13-cis-retinoic acids confirms the correlation between embryonic exposure and teratogenic potency in the mouse. Our results indicate that pharmacokinetic studies are essential for the interpretation of relative teratogenic potencies of retinoids as well as apparent differences between in vivo and in vitro teratogenesis. A free carboxyl group at the terminal end of the tetraene chain was necessary for high activity of the retinoids studied.
比较了单剂量致畸性阿维A酯和依曲替酸的经胎盘药代动力学,特别关注游离酸代谢物阿维A在暴露胚胎中的分布和浓度。还在肢芽间充质细胞“微团”培养试验中测试了这三种芳香族维甲酸对软骨生成的直接抑制作用。在NMRI小鼠妊娠第11天给予100mg/kg的标准剂量后,所有三种化合物均具有致畸性,但它们的效力彼此不同。阿维A酯作为致畸剂最具活性,与我们的标准全反式维甲酸效力相当;每个暴露的胎儿均出现畸形,所有四肢骨骼严重缩短以及腭裂。阿维A的效力低于阿维A酯,依曲替酰胺作为致畸剂的活性明显低于其他两种。在体外试验中,只有阿维A抑制软骨生成,且这种活性与全反式维甲酸相当(IC50为12ng/ml)。阿维A酯和依曲替酰胺(分别含有乙酯和乙酰胺端基)在体外基本无活性,这表明游离羧基可能是体外抑制软骨生成的必要条件。体内和体外结果之间的这些差异可以通过使用HPLC方法的药代动力学研究来解决。阿维A酯和依曲替酰胺在体内均代谢为阿维A,它们可能是共同的致畸代谢物。阿维A酯的高致畸效力可能是其代谢物阿维A在胚胎中高浓度以及AUC值的结果。另一方面,依曲替酰胺相对较低的致畸性可能与阿维A的胚胎峰值水平以及AUC值低约5倍有关。将这些结果与先前获得的全反式和13-顺式维甲酸的结果进行比较,证实了小鼠胚胎暴露与致畸效力之间的相关性。我们的结果表明,药代动力学研究对于解释维甲酸的相对致畸效力以及体内和体外致畸作用之间的明显差异至关重要。所研究的维甲酸的高活性需要四烯链末端有一个游离羧基。