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Cecil H. and Ida Green Center for Reproductive Biology Sciences and the Departments of Obstetrics and Gynecology and Pharmacology, The University of Texas Health Science Center, Southwestern Medical School, Dallas, Texas 75235
Address all correspondence and requests for reprints to: Dr. Leon Milewich, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical School, 5323 Harry Hines Boulevard, Dallas, Texas 75235.
The capacity of endothelial cells from pulmonary arteries and veins to convert dehydroisoandrosterone (3β-hydroxy-5-androsten-17-one) and androstenedione to potent, biologically active steroids was investigated. The metabolites of [3H]dehydroisoandrosterone produced in pulmonary artery endothelial cells were androstenedione and 5-androstene-3β,17β-diol. The metabolites isolated from incubation of pulmonary arterial cells with [3H]androstenedione were testosterone, 5
-androstane-3,17-dione, 5
-dihydrotestosterone (17β-hydroxy-5
-androstan-3-one), isoandrosterone (3β-hydroxy-5
-androstan-17-one), and androsterone. The products of [3H]androstenedione metabolism in human pulmonary venous cells were the same as those formed in arterial cells, and in addition, 5
androstane-3
,17(β-diol and 5
-androstane-3β,17β-diol were formed. The rates of metabolite formation from [3H] androstenedione in pulmonary arterial and venous endothelial cells were linear with incubation time up to 3 h. These findings suggest that the pulmonary endothelium is an important site for the metabolism of dehydroisoandrosterone and androstenedione in the human lung. Endothelial cells produce the same metabolites as human lung tissue, with the exception of hydroxylated steroids. (J Clin Endocrinol Metab 56: 930, 1983)
* This work was supported in part by USPHS Grants AM-27257 and HL-18826.
Received September 2, 1982.
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