Age-Dependent Neurotoxicity in Rats Chronically Exposed to Low Level Lead Ingestion: Phospholipid Metabolism in Synaptosomes and Microvessels

The uptake of [ ³H]Ch and [³H]MI by synaptosomes or microvessels, the concentration of membrane phospholipids, and the incorporation of [ ³H]Ch or [³H]MI into the respective phospholipids in synaptosomes or microvessels, were studied in samples obtained from the brain of control rats and rats exposed to a low-level lead ingestion starting prenatally, neonatally or at an adult age. The V_max values for the uptake of [³H]Ch by control-neonatal and control-adult samples were significantly different. However, there was no significant difference in the V_max values for the uptake of [³H]MI by control-neonatal and control- adult samples. The same was true for the K_m values for the uptake of [³H]Ch or [ ³H]MI. Chronic exposure of embryonic and neonatal rats to a low-level lead ingestion inhibited the rate of uptake of [³H]Ch and [³H]MI by the brain synaptosomes or microvessels, reduced the concentrations of Ch and MI phospholipids in membranes of these tissues, and did not effect the incorporation of [³H]Ch and [³H]MI into the respective membrane phospholipids. In adult rats, these changes were not observed following chronic exposure. These observations suggest that Ch and MI transport mechanisms in the brain of embryonic and neonatal rats are sensitive to chronic low-level lead ingestion but Ch and MI transport mechanisms in the brain of adult rats are not. A lead-induced decrease in the availability of Ch and MI in the brain may be responsible for the observed decrease in the concentrations of phospholipids.