The relative potency of testosterone and dihydrotestosterone in the rat ventral prostate: Role of 5alpha-reductase.
A. Stuart Wright
Abstract
A. Stuart Wright
Abstract
Testosterone (T), the major circulating androgen, must be converted to dihydrotestosterone (DHT) by the enzyme 5alpha-reductase (5alpha-R) for maximal activity in the prostate. Based on its higher affinity for the androgen receptor, its high intraprostatic concentration and the observation that men with congenital 5alpha-R deficiency have small prostates, DHT was considered to be the only active androgen in the prostate. In both rats and men, administration of 5alpha-R inhibitors such as finasteride results in prostate shrinkage but not to the same extent as castration. The most probable reason is the reciprocal rise in intraprostatic T that accompanies the decrease in DHT on 5alpha-R inhibition. The objective of the studies presented here was to investigate the relative potencies of T and DHT in prevention of rat ventral prostate regression and in regrowth.
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Testosterone (T), the major circulating androgen, must be converted to dihydrotestosterone (DHT) by the enzyme 5alpha-reductase (5alpha-R) for maximal activity in the prostate. Based on its higher affinity for the androgen receptor, its high intraprostatic concentration and the observation that men with congenital 5alpha-R deficiency have small prostates, DHT was considered to be the only active androgen in the prostate. In both rats and men, administration of 5alpha-R inhibitors such as finasteride results in prostate shrinkage but not to the same extent as castration. The most probable reason is the reciprocal rise in intraprostatic T that accompanies the decrease in DHT on 5alpha-R inhibition. The objective of the studies presented here was to investigate the relative potencies of T and DHT in prevention of rat ventral prostate regression and in regrowth.
Key concepts: Finasteride, Dihydrotestosterone, Testosterone (patch), Endocrinology, Prostate, Internal medicine, Androgen, Androgen receptor