Congenital malformations induced by rabbit antiserum against rat placental glycoproteins isolated by concanavalin A affinity chromatography. Teratogenic antibodies are not nephrotoxic.

Previous investigations concerning the biologic effects of heterologous antisera raised against rat chorioallantoic placenta demonstrated that the antisera were nephrotoxic, abortifacient, and teratogenic. It is important to determine if maternal nephritis is associated with abnormal embryonic development induced by antiplacenta sera. In this report, a soluble glycoprotein fraction was isolated from rat chorioallantoic placentas of day 16 of gestation by concanavalin A affinity chromatography after solubilizing the saline-washed placental sediment by sodium deoxycholate. Antiserum raised against this soluble glycoprotein fraction induced abnormal embryonic development when the antiserum was injected intraperitoneally into 9th day pregnant rats. The teratogenic effect of the antiserum was dose-dependent. The most frequently observed congenital defect was anophthalmia. Examination of the teratogenic antiserum for nephrotoxicity was performed by measuring the daily urinary protein output of the injected animals and by examining the ultrastructural morphology of the renal glomeruli after the injection of the antiserum into male and pregnant rats. The data indicated that the teratogenic antiserum was not nephrotoxic and therefore support the view that abnormal embryonic development does not result from maternal Masugi nephritis in this experimental model. In vivo immunofluorescent studies demonstrated that the antibodies to the placental glycoproteins localized primarily in the visceral yolk-sac endodermal cells and in Reichert's membrane, which is the basement membrane of the parietal yolk-sac. It is postulated that the antiserum might induce abnormal embryonic development by interfering with the normal functions of the yolk-sac placenta.