Effect of early inorganic lead exposure on rat blood-brain barrier permeability to tyrosine or choline.

The primary objective of this research was to test the hypothesis that low level lead (Pb) exposure during early life leads to disruption in blood-brain barrier (BBB) function in the young rat. Newborn rats received lead via milk from lactating dams that were drinking water containing 0.1% lead acetate Pb(Ac)2. Pups were weaned to, and maintained on, 0.1% Pb(Ac)2-containing solution up to 70 days of age. Growth was no different from that of coetaneous controls. Experimental animals displayed elevated blood lead (15 microgram/dl) within 2 days from the onset of exposure, and it increased to 35-40 microgram/dl between 13 and 22 days of age. Following weaning to the higher lead source, blood lead values continued to increase (55 microgram/dl) but, then, appeared to decline after 55 days of age. Control animals consistently possessed blood lead values of less than 5 microgram/dl. The brain capillary (BBB) transport of the neurotransmitter precursors, choline and tyrosine, was studied at 55 and 70 days of age using intracarotid injections of a bolus containing 14C-labeled substrate and 3HOH as a diffusable reference (Brain Uptake Index). There was no difference in the transport of either choline of tyrosine in lead-intoxicated rats compared to controls. Suspected adverse psychoneurological effects of low level inorganic lead probably relate to the parenchymal cells of the CNS and not to the brain capillary endothelial cells.