Oxidative stress and excess of iron in the brain has been implicated in a variety of acute and chronic neurological conditions. The neonatal period is critical for the establishment of normal iron content in the adult brain. In the present study, the long-term oxidative effects of iron exposure during this period were assessed by treating Wistar rats orally with 0, 7.5 or 15 mg Fe(+2)/kg of body weight on postnatal days 10-12. Thiobarbituric acid reactive species, protein carbonyl, superoxide dismutase activity were measured at the age of 3 months. It was found that there was an increase in thiobarbituric acid reactive species and protein carbonyl in the substantia nigra of iron treated rats. In contrast, oxidative stress in the striatum was decreased. Superoxide dismutase activity was decreased in the substantia nigra iron treated rats. There were no differences in cerebellum measures among the groups. Our results demonstrated that iron supplementation in a critical neonatal period induced oxidative stress and modulated SOD activity in the adult life in selective brain regions.