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The Metabolism and Transplacental Passage of 3H-Vitamin D3 in the Pregnant Primate, Macaca mulatta

In animal system excessive maternal ingestion of vitamin D during pregnancy has been shown to cause in the offspring most of the bony and arterial pathology seen in idiopathic hypercalcamia of infancy. This disease is felt by some to be due to altered responsiveness of the fetus and/or mother to vitamin D. Mammals, including man, convert vitamin D to 25-hydroxy vitamin D before the vitamin has its characteristic effects. A previous study demonstrated nonspecific antirachitic activity in cord serum of rabbits whose mothers had been given massive vitamin D doses during pregnancy. The current study demonstrates not only how much, but also, in what metabolic form the vitamin traverses the placenta.C-sections were performed 6, 24, 48 and 100 h after IV administration of 3H-vitamin D3 in non-physiologic doses to pregnant rhesus monkeys. All tissues within the fetal compartment were studied for the amount and metabolic state of the vitamin present. Results show that the placenta acts as a barrier and storage organ from which the fetal serum somewhat selectively supplies fetal tissues with, mainly, 25-hydroxy vitamin D. Fetal tissues do not appear to convert vitamin D to 25-hydroxy vitamin D. The data suggest that at physiologic doses the fetal tissues would probably not be exposed to unaltered vitamin D. This suggests that the teratogenicity of vitamin D is due to undue exposure of fetal tissues to the unaltered vitamin.