Effects of transitory pteroylglutamic acid (PGA) deficiency on embryonic and placental development in the rat

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Abstract
Female Long‐Evans rats, were given a purified PGA‐deficient diet containing 10 mg% of the antimetabolite, 9‐methyl‐PGA, from days 8 to 10 of gestation, followed by a PGA‐supplemented diet from day 10 to autopsy. Thisregimen resulted in 18% embryonic death by day 11, 65% by day 12, and 100% by day 13 of pregnancy.No morphological differences between PGA‐deficient and control embryos were observed at nine or nine and one‐half days but ten‐day embryos showed retardation of growth and development and decreased mitosis, especially in the neural epithelium. In 11‐day PGA‐deficient embryos the cranial portion of the neural tube was markedly retarded or anomalous. PGA‐deficient embryos still living on day 12 exhibited severely retarded or abnormal development of the cranial region with moderate retardation in other areas. The placentas of PGA‐deficient embryos were normal until the twelfth or thirteenth day when vacuolization and pyknosis of giant cells in the junctional zone occurred. These changes as well as placental involution through day 16 appeared morphologically identical with those observed in placentas of embryosdestroyed surgically on day 12. PGA‐deficiency appeared primarily to affect embryonic rather than placental tissues.