STIMULATIVE EFFECTS OF LEAD ON BONE-RESORPTION IN ORGAN-CULTURE

To clarify whether hypercalcemia after injection of Pb to rats is due to biological bone resorption or physicochemical mineral dissolution, the effect of lead (Pb) on release of previously incorporated Ca-45 in organ culture was investigated, Pb at 50 mu M and above stimulated the release of Ca-45 and hydroxyproline (Hyp). Pb did not stimulate Ca-45 release from the bones inactivated by freezing and thawing. Eel calcitonin (ECT), bafilomycin A(1) and scopadulcic acid B (SDB) inhibited Pb-stimulated Ca-45 release. These results indicate that Pb-induced Ca-45 release is due to osteoclastic bone resorption. Pb-stimulated bone resorption was inhibited by indomethacin and flurbiprofen. Pb stimulated the release of prostaglandin E(2) PGE(2) from the bones into the media. There was significantly high correlation between Ca-45 and PGE(2) release. Pb-induced bone resorption was inferred to be mediated by PGE(2). From these results, it was suggested that hypercalcemia after Pb injection might be caused by biological bone resorption.