Differential binding of 14 C-cortisone in fetal, placental, and maternal liver tissue in A-J and C57BL mice.

The gross teratologic effects of cortisone on the fetal development of mice have been investigated extensively. Cortisone injected into pregnant mice on days 11, 12, 13, and 14 of pregnancy will cause cleft palate without cleft lip at a frequency that is dependent on the maternal and paternal genotypes.1'2 In addition to cortisone, cleft palate can be induced by a large number of environmental conditions and drugs including corticoids, salicylates, vitamin A, and antimitotic agents such as X rays, 6-aminonictinamide, and nutritional deficiencies.3 Although cleft palate is the major structural malformation associated with cortisone administration, other minor embryopathic features including shortening of the head, mandibular alteration, and spina bifida have been reported.4 Correspondingly, increases in resorption, decreases in fetal weight, and increases in cleft palate frequency after cortisone administration point to the fact that a significant change in fetal or maternal metabolism, or both, has occurred.5 These facts tend to support our hypothesis that cortisone affects biochemical events in numerous tissues, and that cleft palate specifically results because of the temporal and spacial vulnerability of palatal closure. It has been suggested that cortisone decreases