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Androstenedione Metabolism in Human Alveolar Macrophages^*

Cecil H. and Ida Green Center for Reproductive Biology Sciences and the Departments of Obstetrics and Gynecology and Internal Medicine, 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 metabolism of [³H]androstenedione by human alveolar macrophages was investigated. Alveolar macrophages were obtained by bronchopulmonary lavage by use of a heparinized saline solution devoid of Ca⁺⁺ and Mg⁺⁺. After purification, the macrophages were incubated at 37 C in RPMI-1640 medium that contained glucose and [l,2,6,7-³H]androstenedione under various experimental conditions. Control incubations were conducted without macrophages. After incubation, ¹⁴C-labeled steroids that corresponded to the metabolites were added as internal recovery standards. The metabolites were characterized by chromatography and crystallization to constant ³H to ¹⁴C ratios. Human alveolar macrophages convert [³H] androstenedione to 5-androstane-3,17-dione, testosterone, 5dihydrotestosterone, androsterone, and isoandrosterone. Unidentified polar metabolites also were formed. Therefore, the following enzymes are present in these cells: 5-reductase, 17β-hydroxysteroid dehydrogenase, 3-hydroxysteroid dehydrogenase, 3β-hydroxysteroid dehydrogenase, and unknown hydroxylase(s).

The rates of formation of the principal metabolites, 5androstanedione and testosterone, remained linear up to 4 h of incubation and with macrophage number up to 1.5 x 10⁷ cells/ml. These findings suggest that alveolar macrophages may be involved in the peripheral metabolism of androstenedione to potent androgens in man. It is possible that androgens, formed from blood-borne androstenedione within alveolar macrophages, may modulate phagocytic and other activities in these cells. (J Clin Endocrinol Metab 56: 920, 1983)

^* This work was supported in part by USPHS Grants AM-27257 and HL/AI-29543.

Received September 30, 1982.

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