Abstract

Adult female Sprague-Dawley rats were exposed to various concentrations of lead acetate for different lengths of time. Six weeks exposure to lead acetate at concentrations of 0, 0.125, 0.25, 0.5, 1, and 2% in the drinking water, gave rise to brain and blood lead levels that were highly correlated with the lead concentration in the drinking water. When animals were exposed to 1% lead acetate for different lengths of time, an apparent delay in the rate of lead transport into the brain was seen during the first day. However, if animals were exposed for longer time periods, brain lead levels increased faster than did the blood levels. Pieces of fetal cortex cerebri were grafted to the anterior eye chamber of host animals exposed to either 1% lead acetate or to sodium acetate. Six weeks after grafting, the lead concentration in the lead-exposed grafts were 31.6 mg/kg dry wt, as compared to 6.4 mg/kg dry wt in sodium acetate control grafts. However, grafts from both groups had lead levels that were approximately five times higher than in cerebral cortex “punches” from corresponding areas of the host brains. Furthermore, zinc and copper levels were also higher in the grafts as compared to punches of in situ cortex. Taken together with previous reports on animal and human lead exposure, these data indicate that oral lead intake in adult rats bearing intraocular brain grafts yields blood and brain levels which are physiologically relevant to problems of clinical lead toxicity.

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