3 days after conception, pregnant Sprague-Dawley rats were fed a diet of galactose + ground lab chow, glucose + ground lab chow, or ground lab chow alone. After delivery, mothers were fed lab chow alone. The offspring were sacrified at 0, 5, 10, 20 and 30 days after birth. Lenses were fixed and processed for light and electron microscopy. Gross observation showed that lenses from offspring of animals fed lab chow or lab chow + glucose were transparent at all times. In contrast, lenses from the offspring of galactose-fed mothers were totally opaque at birth. At 10 and 20 days postpartum the lenses from the offspring of galactose-fed animals displayed opaque regions which were interspersed with transparent areas. Opacities were no longer noted at 30 days postnatal. Thus, at the gross level, the cataracts formed during the period of fetal development appear to be completely reversible. At the ultrastructural level, the overall orientation of the epithelium and the overlying capsule was similar in all lenses examined. However, in the experimental group the fiber membranes were disrupted, and larger inter- and intracellular spaces were noted. The fibers were swollen and contained electron-dense aggregates of variable size. The extent of the galactose-induced damage assessed at the fine structural level regressed as the age of the offspring increased. Lenses and plasma from neonates and mothers were subjected to gas-liquid chromatography for determination of hexoses and polyols. Elevated levels of hexoses and polyols were found in the lenses and plasma of the newborn rats which had been exposed to galactose suggesting that the accumulation of polyols, which triggers cataract formation in older animals, also initiates cataract formation in the newborn.