Abstract
PCA is used often to treat Pb toxicity after administration of CaNa2EDTA. Since the source of Pb mobilized by PCA comes from bone, this study was undertaken to define further PCA's actions on bone, after demonstration of a readily mobile compartment of skeletal Pb in vitro regulated like bone mineral. Pregnant rats were injected with 500 μCi of 203Pb and 200 μCi of 45Ca on the 18th day of pregnancy. On day #19, paired fetal bones were cultured in a chemically defined medium to which PCA, parathyroid hormone (PTH) or 1,25-dihydroxyvitamin D3 (1,25[OH]2D3) were added. For 48 to 120H, bones were maintained in experimental media (EM); and the amount of 203Pb released into the EM's was compared to that released into the appropriate control media (CM). The results (* = p<.01, different from 1.00) were expressed as cpm EM/CM ratios: PCA (1.00mM) 1.96±.04*; PCA+PTH 6.30±.14*; PCA + 1, 25(OH)2 D3 5.89±.10*. Increasing and decreasing medium levels of Ca and phosphate depressed and enhanced 203Pb release, respectively, while no effect on 45Ca release was seen with PCA alone. PCA, compared to equimolar amounts of CaNa2EDTA, was 1000 times less potent in chelating 203Pb; and PCA's maximum effect was transient vs. CaNa2EDTA (48 vs. 120H).
These data indicate that PCA, like CaNa2EDTA, produce 203Pb release from a rapidly mobile compartment of bone Pb; but PCA's action was less potent and short-lived compared to CaNa2EDTA.
Article PDF
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Rosen, J. 265 D-PENICILLAMINE (PCA): ITS ACTIONS ON LEAD-203(203Pb) CHELATION IN BONE ORGAN CULTURE. Pediatr Res 12 (Suppl 4), 408 (1978). https://doi.org/10.1203/00006450-197804001-00270
Issue Date:
DOI: https://doi.org/10.1203/00006450-197804001-00270