ABSTRACT
With the benefit of hindsight H is quite clear that rctinoids must be playing an important role in embryonic development. Vitamin deficiencies, and in particular a deficiency of vitamin A, were the first dietary means of producing congenital malformations of the embryo. InHial experiments, performed as long ago as the 1930s on pigs (1), resulted in 100% of embryos born to a vitamin A-deficient sow showing congenital abnormalities. Such abnormalities have over subsequent decades become characteristically familiar and have been seen in other mam~ maHan species such as rat, rabbit, cattle, sheep, and humans (2). These abnormalities involve defects of the following systems: central nervous system (hydrocephalus, spina bifida), eye (anophthalmia, microphthalmia), face (harelip, cleft palate), dentition, ear (accessory ears, otosclerosis), limb, urinogenital system (cryptorchidism, ectopic ovaries, pseudohermaphroditism, renal defects), skin (subcutaneous cysts), lungs (hypoplasia), heart (incomplete ventricular septation, spongy myocardium, aortic arch defects, aorticopulmonary septal defects, valvulus communis). An additional system affected is the hematopoietic system (failure of circulation and major blood vessels to form), which has only been seen in chick embryos (3).
