Abstract

The concentration of lead in blood and cerebral cortex (Cx), striatum (St), hippocampus (Hc), and midbrain (Mb) was measured by flameless atomic absorption spectrophotometry in rats that had received (po) daily 0.005, 0.025, 0.1, or 1.0 mg lead/kg from 3 days until 4, 6, or 8 weeks of age. The blood lead levels and regional brain lead content of control rats increased with age. In addition to a dose-dependent increase in blood lead levels of rats exposed to 0.1 mg lead/kg (by 176%) and 1.0 mg lead/kg (by 396%), the concentration of the metal in blood of rats treated with the 0.1 mg/kg dose initially increased with the duration of exposure, reached a maximum value of 13.8 μg/dl at 6 weeks of age, and leveled off thereafter. Whereas exposure to small amounts of lead (0.025 mg/kg) resulted in a preferential accumulation of lead in the Hc (by 127%), a larger dose of the metal (0.1 mg/kg) administered for the same period of time produced significant increases in the lead content of the Cx (by 80%), St (by 106%), Hc (by 134%), and Mb (by 67%); no significant interregional differences in lead content were noted. The duration of treatment also influenced the distribution of lead. Exposure to 0.1 mg lead/kg for 4 weeks resulted in a significant increase in the lead levels of only the Cx (by 125%) and Hc (by 522%), while the same treatment for 8 weeks resulted in a significant and similar accumulation of lead in all of the regions examined. These data indicate that in the case of chronic low-level lead poisoning, brain regional lead distribution is influenced by both the dose of the metal administered and the duration of exposure. Significant amounts of lead persisted in brain tissue for as long as 2 and 4 weeks after the withdrawal of lead treatment.

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