Abstract
PROSTAGLANDINS are potent bone resorbers1 which have been implicated as mediators of bone loss and hypercalcaemia in disease2–6, but the specific products in the pathway of prostaglandin synthesis and degradation which are responsible have not yet been identified in vivo. Although PGE2 is the most potent stimulator of bone resorption among the prostaglandins thus far tested in vitro1, in animal tumour models, the increase in immunoreactive PGE2 concentrations does not correlate well with the development of hypercalcaemia2. We therefore tested the early products of arachidonic acid metabolism via the cyclo-oxygenase pathway, the prostaglandin endoperoxides (PGG2 and PGH2) and some of the 13,14-dihydro (H-PGE2 and Ha-PGE2) and 15-keto-13,14-dihydro metabolites of prostaglandins (15K-H2-PGE2 and 15K-H-PGF2α) for their effects on the release of previously incorporated 45Ca from cultured foetal rat long bones. The endoperoxides were found to cause a rapid transient increase in the release of previously incorporated 45Ca from bone, but did not stimulate prolonged resorption. H2-PGE2 and H2-PGE1 were almost as potent as the parent compounds. 15K-H2-PGE2 and 15K-H-PGF2α were much less potent, but did stimulate resorption at 10−5 M.
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RAISZ, L., DIETRICH, J., SIMMONS, H. et al. Effect of prostaglandin endoperoxides and metabolites on bone resorption in vitro. Nature 267, 532–534 (1977). https://doi.org/10.1038/267532a0
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DOI: https://doi.org/10.1038/267532a0
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