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Free access | 10.1172/JCI106392
Department of Internal Medicine, The University of Texas Southwestern Medical School at Dallas, Dallas, Texas 75235
Department of Obstetrics and Gynecology, The University of Texas Southwestern Medical School at Dallas, Dallas, Texas 75235
Department of Biochemistry, The University of Texas Southwestern Medical School at Dallas, Dallas, Texas 75235
Find articles by Gloyna, R. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, The University of Texas Southwestern Medical School at Dallas, Dallas, Texas 75235
Department of Obstetrics and Gynecology, The University of Texas Southwestern Medical School at Dallas, Dallas, Texas 75235
Department of Biochemistry, The University of Texas Southwestern Medical School at Dallas, Dallas, Texas 75235
Find articles by Siiteri, P. in: JCI | PubMed | Google Scholar
Department of Internal Medicine, The University of Texas Southwestern Medical School at Dallas, Dallas, Texas 75235
Department of Obstetrics and Gynecology, The University of Texas Southwestern Medical School at Dallas, Dallas, Texas 75235
Department of Biochemistry, The University of Texas Southwestern Medical School at Dallas, Dallas, Texas 75235
Find articles by Wilson, J. in: JCI | PubMed | Google Scholar
Published September 1, 1970 - More info
Three types of studies have been performed in immature, mature, and hypertrophic prostate glands of the dog. First, the concentrations of testosterone and dihydrotestosterone have been measured in the three types of gland. Dihydrotestosterone was the predominant hormone recovered in all prostates studied and was present in approximately five times higher concentration in the hypertrophic as compared to the other types of dog prostate. Second, pharmacological doses of dihydrotestosterone were administered to castrated dogs for 9 months and resulted in a distinct acceleration of prostatic growth as compared to testosterone treatment. Third, the rates of formation and degradation of dihydrotestosterone were measured in normal and hypertrophic tissue and were found to be essentially the same. These observations suggest that dihydrotestosterone accumulation may be causally linked to the development of canine prostatic hypertrophy. However, the mechanism by which dihydrotestosterone accumulates in the prostate remains to be determined.
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