Characteristics of the inhibitory effect of chronic treatment with an LHRH agonist on testicular steroidogenesis in the dog

Publisher Website
Google Scholar
Abstract
Daily subcutaneous administration for 3 months of the potent LHRH agonist (D‐Ser(TBU)6, des‐Gly‐NH210) LHRH ethylamide (25 μg) to adult dogs having spontaneous benign prostate hyperplasia (BPH) causes a marked inhibition of testicular androstenedione and testosterone secretion. This inhibition of Δ4‐androgen secretion is accompanied by a decrease of testicular progestin precursors and 5α‐androgen metabolites, thus suggesting that, in dog, the loss of testicular steroidogenic activity, induced by the administration of an LHRH agonist, is due to a total inhibition of testicular steroidogenesis. In plasma, the concentration of both testosterone and dihydrotestosterone is also markedly depressed while androstane‐3α, 17β‐diol levels remain unchanged. Measurement of prostatic steroid content has shown that administration of the LHRH agonist as well as castration is associated with a marked decrease in androstenedione, testosterone, and dihydrotestosterone levels in prostate while there is a small inhibition of androst‐5‐ene‐3β,17β‐diol, androstane‐3β,17β‐diol, dehydroepiandrosterone, and estrone concentrations in this tissue. The present data show that treatment with an LHRH agonist in the dog causes a marked inhibition of testicular steroid secretion similar to the one observed in adult men, and suggest that steroids from adrenal origin may also be involved in prostatic function.

This publication has 19 references indexed in Scilit: