Stimulative effects of lead on bone resorption in organ culture

• Published in: Toxicology (Amsterdam) 1995-03, Vol.97 (1), p.191-197
• Main Authors: Miyahara, Tatsuro, Komiyama, Hiroko, Miyanishi, Atsuko, Takata, Masakazu, Nagai, miyuki, Kozuka, Hiroshi, Hayashi, Toshimitsu, Yamamoto, Masako, Ito, yusuke, Odake, Hiroshi, Koizumi, Fumitomo
• Format: Article
• Language: English
• Subjects: Animals; Anti-Bacterial Agents - pharmacology; Biological and medical sciences; Bone resorption; Bone Resorption - chemically induced; Calcitonin; Calcitonin - pharmacology; Calcium - metabolism; Chemical and industrial products toxicology. Toxic occupational diseases; Dinoprostone - biosynthesis; Hydroxyproline; Hydroxyproline - metabolism; Lead; Lead - toxicity; Macrolides; Medical sciences; Metals and various inorganic compounds; Mice; Organ Culture Techniques; Osteoclast; Prostaglandin E 2; Toxicology
• ISSN: 0300-483X; 1879-3185
• DOI: 10.1016/0300-483X(94)02948-T

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