Abstract
In animals, fetal development and growth are altered by maternal vitamin A deficiency. Severely deficient pregnant animals experience complications of gestation and often resorb or abort their fetuses, or they produce offsprings with congenital abnormalities affecting several organ systems (Wallington and Underwood, 1986). Newborn and weanling rats fed diets deficient in vitamin A maintain normal growth for a period of weeks then their growth slows, plateaus and declines. These are classic observations in experimental studies conducted in several animal species, and for many years were the basis for the biological assay of vitamin A potency and nutritional adequacy (Moore, 1957). This fact also is the basis for setting basal dietary requirements linked to growth rate throughout the life cycle (FAO/WHO, 1988).