Effect of an LHRH Agonist and hCG on Testicular Steroidogenesis in the Adult Rat

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Abstract
A dose-dependent inhibition of testicular LH and prolaction binding was observed after 9 days of daily administration of 1, 5, 10, 50 or 250 ng of the LHRH agonist [D-Ala6, des-Gly-NH210] LHRH ethylamide. In addition, desensitization of testes was studied by radioimmunoassay of testicular and plasma steroid intermediates. When basal testicular steroid levels were measured, it was found that the progesterone concentration remained relatively normal with 17-OH-progesterone, and, to a greater extent, androstenedione and testosterone levels were decreased after treatment with 10 ng agonist per day. A maximal inhibitory effect was observed at the 50 or 250 ng doses, thus suggesting an enzymatic defect at the level of 17-hydroxylase and 17, 20-desmolase activities. When testicular steroid levels were measured 2 h after injection of 10 μg of oLH, we observed that in animals treated with 50 or 250 ng of the LHRH analogue the response of testicular progesterone concentration was only slightly decreased, whereas the 17-OH-progesterone, androstenedione and testosterone responses were almost completely inhibited. By contrast, low doses of the LHRH agonist (1 or 5 ng) induced a stimulation (up to 100% above control levels) of the steroidogenic response to oLH. We next compared the effect of single treatment with the LHRH agonist or with hCG. A single injection of the LHRH agonist induced, after 3 days, a 50% decrease of basal levels of testicular testosterone and its precursors except for progesterone which was stimulated to 150% above control levels and estradiol which remained unchanged. However, a single injection of hCG led to an approximately 100% stimulation of levels of testicular steroids except for progesterone which was 700% above control levels. When the steroidogenic response to oLH was measured, treatment with hCG or the LHRH agonist led to stimulation of steroidogenesis up to progesterone formation. Although the extent of the enzymatic defects is dependent upon the dose and schedule of administration, both hCG and the LHRH agonist exert inhibitory effects at the level of 17-hydroxylase and 17, 20-desmolase activities.