The Effects of Mesterolone on the Male Accessory Sex Organs, on Spermiogram, Plasma Testosterone and FSH

Andrologia ◽  
2009 ◽  
Vol 10 (4) ◽  
pp. 299-306 ◽  
Author(s):  
V. NIKKANEN
1983 ◽  
Vol 104 (2) ◽  
pp. 246-252 ◽  
Author(s):  
M. C. Viguier-Martinez ◽  
M. T. Hochereau de Reviers ◽  
B. Barenton ◽  
C. Perreau

Abstract. Adult male Wistar rats were treated with flutamide from 90 to 105 days of age. In a first experiment, testis and accessory sex organs were weighed. In the same animals, hypothalamic LRH content, pituitary gonadotrophin concentrations, plasma LH, FSH, prolactin and testosterone levels, and testicular gonadotrophin receptors were evaluated. In a second experiment, fertility was tested at the end of the treatment, and histology of the testis was performed. All the results were compared to those obtained in control animals of the same age. Accessory glands of genital tract were significantly lower in flutamide-treated animals (P < 0.01). Hypothalamic LRH, pituitary and plasma FSH, and prolactin concentrations were unchanged, while pituitary and plasma LH level and especially plasma testosterone concentration were increased (P < 0.001). Flutamide therefore exerted a strong inhibition on testosterone-dependent organs, and blocked the negative feedback of testosterone on the hypothalamo-pituitary axis, increasing the LH levels. Testis weight, intertubular tissue volume, total number and total volume of Leydig cells/testis, as well as total length and diameter of seminiferous tubules were unchanged in flutamide treated rats. However number of LH receptors/Leydig cell, nuclear area of Sertoli cells, number of FSH receptors/Sertoli cell, number of leptotene spermatocytes and of round spermatids per cross section, and yield of spermatogonial divisions were decreased after treatment. Flutamide treatment also decreased fertility by 48% (P < 0.05). This lowered fertility is likely the result of impaired spermatogenesis and/or a dysfunction of accessory sex organs.


1986 ◽  
Vol 112 (4) ◽  
pp. 595-602 ◽  
Author(s):  
Th. Lemarchand-Béraud ◽  
V. Jaussan ◽  
M. G. Zürich

Abstract. LRH and its agonists have been shown to exert both stimulatory and inhibitory effects on testicular function. In the present study, the dose and length of treatment were tested to determine the appearance of the stimulatory and inhibitory effects of LRH agonist on testicular axis including the three levels. Two doses of an agonist of LRH, 40 and 100 ng/100 g body weight (buserelin, 'agonist'), were administered daily for 1 to 15 days to adult male rats. Control rats received the vehicle only. On day 1, 2, 4, 8 and 15 of treatment, the pituitary, testicular and peripheral levels (weight of accessory sex organs and androgen receptors in ventral prostate) were tested 6 h after the last injection. For the 15 days of treatment with both doses, a stimulatory effect of the 'agonist' was observed on LH and FSH release. A short exposure (1–2 days) to the low dose of the 'agonist' had a stimulatory effect on the density of LH/hCG testicular receptors (326 ± 49 vs control 185 ± 2 1 fmol/mg protein, mean ± sem), on the weights of seminal vesicles and ventral prostate and exposure to both doses led to high plasma testosterone levels (13.8 ± 0.5 and 13.7 ± 0.7 ng/ml, respectively, vs control 2.6 ± 0.3 ng/ml), and to an increased density of nuclear androgen receptors in the ventral prostate (142 ± 9 and 144 ± 15 fmol/mg protein respectively vs control 97 ± 12 fmol/mg protein). A prolonged exposure (4–15 days) to both doses of the 'agonist' had a time-dependent inhibitory effect on the density of LH/hCG testicular receptors, the weight of testes, seminal vesicles and ventral prostate. It had no effects on plasma testosterone levels and on the density of nuclear ardrogen receptors in the ventral prostate. These data show that exposure to low doses of the 'agonist' for a short time leads to a stimulatory effect on the pituitary testicular axis in the adult rat, whereas a more prolonged treatment results into a partial inhibition of this axis affecting first the testicular level then the peripheral level but without decreasing the density of androgen receptors in the ventral prostate.


1971 ◽  
Vol 68 (3) ◽  
pp. 576-584 ◽  
Author(s):  
K. O. Nilsson ◽  
B. Hökfelt

ABSTRACT Metyrapone was administered either orally, 750 mg every four h, in a total of six doses, or intravenously 30 mg per kg body weight as a four h infusion. In three males with normal endocrine functions, metyrapone given orally or intravenously induced a fall in plasma testosterone and an elevation of androstenedione within 2–8 h. When metyrapone was administered to a patient given dexamethasone to suppress endogenous ACTH production, the androstenedione levels did not alter whereas the testosterone levels showed a slight, transient decrease. In two normal females metyrapone administration was followed by a marked increase in plasma androstenedione whereas testosterone showed only a minor, gradual increase. In one male patient with Addison's disease the basal plasma testosterone was normal whereas the level of androstenedione was low. Following metyrapone intravenously, there was a slight suppression of plasma testosterone but no change in the androstenedione concentration. In one patient with primary hypogonadism, two with secondary hypogonadism and two with Klinefelter's syndrome the plasma testosterone was low under basal conditions and did not change following metyrapone. Basal plasma androstenedione was within the range for normal males and increased markedly following metyrapone in all the cases.


1972 ◽  
Vol 70 (2) ◽  
pp. 342-350 ◽  
Author(s):  
M. A. Kirschner ◽  
D. W. R. Knorr

ABSTRACT An attempt was made to suppress production of androgens and oestrogens in normal men by administering large doses of exogenous androgens and corticoids. After 5 days of 40 mg fluoxymesterone qd, plasma testosterone concentrations decreased from 509 to 73 ng/100 ml (85%); on adding 8 mg qd of dexamethasone, there was a further decrease to 45 ng/100 ml. Androstenedione concentrations were decreased equally by fluoxymesterone and corticoids. To monitor the suppressive effects of exogenous steroids, urinary LH was followed serially by radioimmunoassay, and decreased to only 40% of control levels after 5 days of fluoxymesterone, with no further suppression noted on adding dexamethasone. Nanogram quantities of steroidal metabolites were not adsorbed by kaolin extraction of urine, thus enabling gonadotrophins (kaolin extract) and low-level steroids (supernate) to be measured in the same urine sample. Urinary oestrone and oestradiol excretion decreased during 5 days of fluoxymesterone, and continued to fall when dexamethasone was added. In no case was oestrone or oestradiol excretion, urinary LH or plasma androgens completely suppressed by large doses of fluoxymesterone alone, or in combination with large doses of dexamethasone.


1981 ◽  
Vol 96 (2) ◽  
pp. 273-280 ◽  
Author(s):  
Mridula Chowdhury ◽  
Robert Tcholakian ◽  
Emil Steinberger

Abstract. It has been suggested that treatment of intact male rats with oestradiol benzoate (OeB) causes an interference with testosterone (T) production by the testes by a direct inhibitory effect on steroidogenesis. To test this hypothesis, different doses (5, 10 or 25 IU) of hCG were administered concomitantly with 50 μg of OeB to adult intact or hypophysectomized male rats. The testicular and plasma testosterone, and serum hCG levels were determined. The sex accessory weights were recorded. In the intact OeB-treated group of animals, hCG stimulated both the secondary sex organs and plasma testosterone levels above the intact control group. However, in hypophysectomized animals, although plasma testosterone levels increased above that of intact controls, their secondary sex organ weights did not. Moreover, inspite of high circulating hCG levels, the testicular testosterone content and concentration remained suppressed in OeB-treated animals. The reason for such dichotomy of hCG action on OeB-treated animals is not clear at present.


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