To determine the susceptibility of developing brain and other tissues to accumulate zinc, rats were exposed to zinc at different periods of ontogeny. For the prenatal group, pregnant Wistar rats received 50 ppm of zinc (ZnSO4 · 7H2O) in drinking for the entire duration of pregnancy. On the day of delivery zinc was removed from the drinking water. Another group, dams, received 50 ppm of zinc in drinking water only during the suckling period (from delivery until the 21st day of postnatal life). Their offspring were weaned on the 21st day, at which time zinc was removed from the drinking water. The control group drank tap water only. At 3 weeks after birth, the level of zinc was estimated in the brain, liver, mandibular bone and kidney of offspring from all groups. At 8 weeks after birth 6-[3H]D-glucose (500 μCi/kg) was administered IP to male offspring, 15 minutes before sacrifice. By liquid scintillation spectroscopy, 3H-activity (expressed as disintegrations per minute [DPM]) was determined in discrete parts of the brain and some peripheral tissues, and expressed as DPM/100 mg of tissue, wet weight. It was found that the highest amount of zinc was accumulated in the brain and liver of rat offspring that were exposed to zinc postnatally. [3H]-activity was at lower levels, in comparison, in nearly all other parts of the brain of rats exposed to zinc postnatally. In offspring receiving zinc prenatally, zinc levels were at similar or lower amounts in the brain and peripheral tissues, vs. the group with postnatal exposure. From this study in rats we conclude that zinc accumulates to the highest extent in brain, following a later ontogenetic (postnatal) exposure period, and by this, there is also greater disturbance of metabolic processes associated with glucose utilization.