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Aromatase Activity in a Rat Leydig Cell Tumor^*

Departments of Medicine and Obstetrics and Gynecology, University of Massachusetts Medical Center Worcester, Massachusetts 01605

Address all correspondence and requests for reprints to: C. Longcope, Department of Ob/Gyn, University of Massachusetts Medical Center, 55 Lake Avenue North, Worcester, Massachusetts 01605.

Abstract

Male Wistar-Furth rats bearing the transplantable LTW(m) Leydig cell tumor have elevated serum estradiol (E₂) concentrations. We measured the ability of these tumors to aromatize testosterone (T) to E₂ by two methods. First, tumor minces were incubated with [7–³H]T, and the resultant [³H]E₂ and [³H]estrone were purified and measured. In addition, tumor cell cultures were incubated with [1β–³H]T, and the resultant [³H]H₂O was determined as a measure of aromatization. Tumor minces aromatized more actively than normal rat testicular tissue (3.30 ± 0.15% of the T added was converted to E₂ by the tumor vs. 0.30 ± 0.25% by normal testis). Most of the aromatizing activity was localized to the microsomes. Using cell cultures the maximum velocity was 6.1 pmol/h-5 x 10⁵ cells, and the K_m was 98 nM. In neither minces nor cell cultures were we able to show stimulation of aromatization with hCG, (Bu)₂cAMP, or phorbol esters, although we could show stimulation by these agents in normal testicular cells. We were unable to inhibit the aromatase activity with human β-endorphin or stimulate it with naloxone. However, we were able to inhibit the aromatase activity with 4- hydroxy-4-androstene-3,17-dione. We conclude that the LTW(m) rat Leydig cell tumor has an active autonomous aromatase system that is not responsive to compounds affecting the adenylate cyclase-cAMP system. It can be inhibited by 4-hydroxy-4-androstene-3,17-dione, a competitive- suicide inhibitor of the aromatase enzyme(s). (Endocrinology 120: 1482–1489,1987)

Footnotes

^* This work was supported by Grants HD-15443, AM-32520, and AM-07302.

Received July 10, 1986.