| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Division of Endocrinology, Department of Medicine, Dalhousie University (R.S.R., D.L.T.) Halifax, Nova Scotia, B3J 2H6 Canada
Canada; Hazelton Biotechnologies Corporation (S.L.) Vienna, Virginia 22180
The Developmental Endocrinology Branch, National Institutes of Child Health and Human Development, National Institutes of Health, (D.L.L.) Bethesda, Maryland 20892
Address all correspondence and requests for reprints to: Roger S. Rittmaster, M.D., Department of Medicine, Halifax Infirmary, 1335 Queen Street, Halifax, Nova Scotia, B3J 2H6 Canada.
3
-Androstanediol glucuronide (Adiol G) is a major metabolite of dihydrotestosterone (DHT). Adiol G actually represents 2 different compounds, since the glucuronide can be conjugated at the 3-carbon position (Adiol 3-G) or at the 17-carbon position (Adiol 17-G). To determine which glucuronide represents the predominant physiological DHT metabolite and which isomer is the major circulating form, we developed a RIA to directly measure Adiol 3-G in serum extracts. In 10 normal men, mean serum Adiol 3-G and total Adiol G levels were 4.44 ± 0.49 (±SE) nmol/L (208 ± 23 ng/dL) and 27.9 ± 2.8 nmol/L (1310 ± 129 ng/dL), respectively (13.9 ± 3.0% of Adiol G was Adiol 3-G). In 10 normal women sampled during the early follicular phase, mean serum Adiol 3-G and total Adiol G levels were 2.64 ± 0.64 nmol/L (124 ± 30 ng/dL) and 14.9 ± 1.5 nmol/ L (697 ± 69 ng/dL), respectively (17.4 ± 3.6% of Adiol G was Adiol 3-G). In 4 normal men infused for 8 h with tritiated DHT, 17.4 ± 3.4% of the resulting tritiated Adiol G was Adiol 3-G. These results indicate that Adiol 17-G is the predominant circulating form of Adiol G in normal men and women and that it is also the major Adiol G isomer derived from DHT.
* This work was supported by a grant from the University Internal Medicine Research Foundation, Dalhousie University, and Grant MA-9619 from the Medical Research Council of Canada. Presented in part at the 69th Annual Meeting of The Endocrine Society, Indianapolis, IN 1987 (Abstract 769).
Received June 12, 1987.
This article has been cited by other articles:
![]() |
Y. Jin, L. Duan, S. H. Lee, H. J. Kloosterboer, I. A. Blair, and T. M. Penning Human Cytosolic Hydroxysteroid Dehydrogenases of the Aldo-ketoreductase Superfamily Catalyze Reduction of Conjugated Steroids: IMPLICATIONS FOR PHASE I AND PHASE II STEROID HORMONE METABOLISM J. Biol. Chem., April 10, 2009; 284(15): 10013 - 10022. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. Hormones and Prostate Cancer Collaborative Group Endogenous Sex Hormones and Prostate Cancer: A Collaborative Analysis of 18 Prospective Studies J Natl Cancer Inst, February 6, 2008; 100(3): 170 - 183. [Abstract] [Full Text] [PDF] |
||||
![]() |
T. Kuuranne, M. Kurkela, M. Thevis, W. Schanzer, M. Finel, and R. Kostiainen GLUCURONIDATION OF ANABOLIC ANDROGENIC STEROIDS BY RECOMBINANT HUMAN UDP-GLUCURONOSYLTRANSFERASES Drug Metab. Dispos., September 1, 2003; 31(9): 1117 - 1124. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |