Stimulative effects of lead on bone resorption in organ culture
| Autor: | Hiroshi Odake, Hiroko Komiyama, Masako Yamamoto, Masakazu Takata, Toshimitsu Hayashi, Tatsuro Miyahara, Atsuko Miyanishi, Miyuki Nagai, Hiroshi Kozuka, Fumitomo Koizumi, Yusuke Ito |
|---|---|
| Rok vydání: | 1995 |
| Předmět: |
Calcitonin
medicine.medical_specialty chemistry.chemical_element Calcium Toxicology Organ culture Bone resorption Dinoprostone Hydroxyproline chemistry.chemical_compound Mice Organ Culture Techniques Osteoclast Internal medicine medicine Animals Prostaglandin E2 Bone Resorption Resorption Anti-Bacterial Agents Endocrinology medicine.anatomical_structure chemistry Lead Macrolides medicine.drug |
| Zdroj: | Toxicology. 97(1-3) |
| ISSN: | 0300-483X |
| Popis: | 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 microM 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 A1 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 E2 (PGE2) from the bones into the media. There was significantly high correlation between 45Ca and PGE2 release. Pb-induced bone resorption was inferred to be mediated by PGE2. From these results, it was suggested that hypercalcemia after Pb injection might be caused by biological bone resorption. |
| Databáze: | OpenAIRE |
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