Neonatal rats were given aqueous lead acetate intragastrically from d 2-20 of life at doses of 0, 10, 50, and 225 mg Pb/kg. Blood Pb concentrations on d 21 were (mean ± SE) 23 ±3 (control), 63 ± 19, 246 + 55, and 994 ± 223 μg/100 ml, and brain Pb concentrations were 14 ± 2, 60 ± 5, 114 ± 15, and 275 ± 26 μg/100 g, respectively. Growth was significantly depressed only in rats given the highest dose of Pb (225 mg/kg.). Solvent-ex tractable lipofuscin pigment concentration of brain tissue progressively decreased over the 21-d duration of the experiment but was not significantly altered at any dose of Pb. Brain glutathione peroxidase, glucose-6-phosphate dehydro-genase, and 6-phosphogluconate dehydrogenase activities were stimulated on d 20 at the maximal dose of Pb, but the activities of brain superoxide dismutases and catalase were not altered by Pb exposure. Locomotor activity was significantly increased in the male animals on d 20, but only at the highest dose of Pb. These results indicate that Pb toxicity in neonatal rats is not associated with accelerated in vivo lipid peroxida-tion in the brain, but that certain oxidant defense mechanisms in the brain are stimulated by Pb.