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·d. 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·d). 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 dehydrogenase, 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 peroxidation in the brain, but that certain oxidant defense mechanisms in the brain are stimulated by Pb.
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