Effects of hydrocortisone on the hypercalcemia and plasma levels of 13,14-dihydro-15-keto-prostaglandin E2 in mice bearing the HSDM1 fibrosarcoma |
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Authors: | Armen H Tashjian Edward F Voelkel Lawrence Levine |
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Institution: | 1. Laboratory of Pharmacology, Harvard School of Dental Medicine, Boston, MA 02115 USA;2. Department of Pharmacology, Harvard Medical School, Boston, MA 02115 USA;3. Department of Biochemistry, Brandeis University, Waltham, MA 02154 USA |
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Abstract: | In mice bearing the prostaglandin-producing HSDM1 fibrosarcoma, the plasma concentration of 13,14-dihydro-15-keto-PGE2 was elevated before the development of hypercalcemia, and the magnitude of the rise was greater than that of PGE2. When hydrocortisone, which inhibits synthesis of PGE2 by HSDM1 cells in culture, was administered to tumor-bearing mice, the steroid hormone prevented the rises in plasma PGE2 metabolite and calcium concentrations. At the dose levels used, hydrocortisone did not inhibit the calcium-mobilizing action of parathyroid hormone or the bone resorption-stimulating activity of . These findings are consistent with our hypothesis that the hypercalcemic syndrome in HSDM1 tumor-bearing mice is due to the secretion of PGE2 by the tumor. |
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