Stimulative effects of lead on bone resorption in organ culture

Abstract 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 45 Ca in organ culture was investigated. Pb at 50 μM and above stimulated the release of 45 Ca and hydroxyproline (Hyp). Pb did not stimulate 45 Ca release from the bones inactivated by freezing and thawing. Eel calcitonin (ECT), bafilomycin A 1 and scopadulcic acid B (SDB) inhibited Pb-stimulated 45 Ca release. These results indicate that Pb-induced 45 Ca 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 45 Ca 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.