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S Caron

Publications and source records attributed to S Caron.

50 records · Page 3Linked to original sources
PubMed1989

Influence of diet on plasma steroids and sex hormone-binding globulin levels in adult men.

Several experimental studies have suggested that diet can alter the production and metabolism of steroids in men. The purpose of this study was to determine the levels of unconjugated steroids and steroid glucuronides as well as sex hormone-binding globulin (SHBG) among normal adult men who were either omnivorous or vegetarians. The participants were white volunteers ranging from 25-35 years of age and the blood samples were taken between 0900 h and 1000 h and between 1600 h and 1700 h for two consecutive days. No significant statistical change was found in plasma dehydroepiandrosterone, dehydroepiandrosterone sulfate, testosterone, dihydrotestosterone and estradiol levels. Vegetarian group showed a higher levels of sex hormone-binding globulin (SHBG) while the free androgen index (FAI; calculated by the ratio testosterone/SHBG) was lower in this group. Although the concentrations of androsterone glucuronide were higher in vegetarian group, the vegetarians had a 25-50% lower level of androstane-3 alpha, 17 beta-diol glucuronide and androstane-3 beta,17 beta-diol glucuronide. Our data further indicate that both, androstane-3 alpha,17 beta-diol glucuronide and androstane-3 beta,17 beta-diol glucuronide concentrations are significantly correlated with SHBG levels and with the FAI values. The increases in androstane-3 alpha,17 beta-diol glucuronide and androstane-3 beta,17 beta-diol glucuronide levels in the omnivorous group are probably a consequence of the elevation of the FAI. Our data suggest that in a vegetarian group, less testosterone is available for androgenic action.

Adult↗
PubMed1989

Local effect of the rabbit embryo-foetus on uterine progesterone and pregnenolone levels.

Rabbit peripheral serum and uterine tissue (embryonic (EZ) and interembryonic (IEZ) zones) were assayed for the main C21, C19 and C18 steroids throughout pregnancy and pseudopregnancy (PSPG). Pregnenolone concentrations in PSPG and IEZ were comparable and remained relatively stable, while its level in EZ increased, reaching a peak value of 18.2 +/- 0.8 ng/g by day 15, and decreasing thereafter to a level comparable to oestrus by day 25. Tissue concentrations of progesterone were comparable in PSPG and IEZ, reached their maximal level on days 6.5 and 9, and decreased significantly (P less than 0.01) on day 15. In EZ, progesterone level was significantly lower than in IEZ and decreased on day 9 compared to day 6.5. A further decrease was observed from days 9 to 15 but no difference between tissues was observed on the latter day. Thus, the blastocyst-foetus exerts a local effect by decreasing progesterone content and increasing pregnenolone level in the uterine tissue adjacent to its implantation (EZ). The conversion of progesterone in uterine tissue to less-active metabolites does not appear to occur towards the C19 and C18 steroids.

Animals↗
PubMed1988

The rise in testicular androgens during the first days of treatment with an LHRH agonist in the dog can be blocked by aminoglutethimide or ketoconazole.

Up to day 6 of treatment of adult dogs, daily subcutaneous administration of 50 micrograms of the LHRH agonist [D-Trp6, des-Gly-NH2-10]LHRH ethylamide causes up to a 3-fold increase in serum testosterone (T) concentration which is followed by a progressive decrease to castration levels (less than or equal to 0.2 ng/ml) at later time intervals (up to 21 days, the last time interval studied). Both aminoglutethimide and ketoconazole, two inhibitors of steroid biosynthesis, cause a 30-40% rise in serum T when administered alone. However, either drug administered in combination with the LHRH agonist completely blocks the transient rise in serum T observed when the LHRH agonist is administered alone. On the other hand, the LHRH agonist prevents the secondary rise in steroid secretion observed when either of the two inhibitors of steroid secretion is used alone. Administration of the pure antiandrogen Flutamide alone or in combination with LHRH-A and an inhibitor of steroid biosynthesis does not influence serum T levels. When the serum levels of pregnenolone, 17-OH-pregnenolone, progesterone, 17-OH-progesterone, dehydroepiandrosterone (DHEA), androstenedione (delta 4-dione), androst-5-ene-3 beta, 17 beta-diol (delta 5-diol), T, dihydrotestosterone (DHT), androstane-3 alpha, 17 beta-diol, androstane-3 beta. 17 beta-diol and 17 beta-estradiol (E2) are analyzed in detail, it can be seen that both aminoglutethimide and ketoconazole not only prevent the rise in serum steroids observed during the first 8 days of treatment with the LHRH agonist but that both compounds enhance the inhibitory effect of the LHRH agonist at later time intervals. A predominant inhibitory effect of ketoconazole is exerted on 17,20-desmolase activity. Aminoglutethimide has little influence on the loss of serum LH bioactivity induced by the LHRH agonist while ketoconazole stimulates the concentration of serum bioactive LH in the absence or presence of simultaneous treatment with the LHRH agonist. The present data clearly demonstrate that aminoglutethimide or ketoconazole can prevent the rise in serum androgens accompanying the first days of treatment with an LHRH agonist in the dog. Moreover, after 3 weeks of treatment, the inhibitory effect of the LHRH agonist on serum androgen levels is enhanced by addition of aminoglutethimide or ketoconazole. Moreover, Flutamide does not interfere with the inhibitory action of the LHRH agonist, aminoglutethimide or ketoconazole, thus suggesting that maximal inhibition of androgen action is likely to be achieved by a combination of these drugs.

Aldehyde-Lyases↗
PubMed1987

Effects of flutamide, a pure antiandrogen, on endocrine parameters, in the adult female rat.

Since antiandrogens having mixed agonistic-antagonistic activities on the androgen receptor have shown benefits in the treatment of hirsutism, the availability of a pure antiandrogen is of particular interest. As a first step, we have thus investigated in detail the effect of the pure antiandrogen Flutamide on endocrine parameters in the female rat. Treatment with the antiandrogen (5 mg, twice daily) for 4 cycles did not affect the 4-day estrous cycle. The antiandrogen had no significant effect on the ovarian level of cytosolic total and available as well as nuclear estrogen receptors in the uterus, and did not affect the concentration of LH and FSH ovarian receptors. The ovarian level of progestins was minimally affected or unchanged on estrus and diestrus I, while an increase was observed under treatment with Flutamide on diestrus II and proestrus. In the plasma, however, there was small or no effect of Flutamide treatment on the concentration of pregnenolone, 17-OH pregnenolone, progesterone and 17-OH-progesterone. The ovarian levels of testosterone (T) and of its two metabolites androstane-3 alpha,17 beta-diol and androstane-3 beta,17 beta-diol were increased by treatment with Flutamide on the morning of diestrus II and proestrus. This was reflected by a 30-100% increase of the levels of plasma T on proestrus. The increase in the ovarian concentration of 5-androstene-3 beta,17 beta-diol (delta 5-diol) and androstenedione observed on diestrus II and on proestrus did not lead to any change in the plasma level of these steroids, which remained normal throughout the estrous cycle during treatment with Flutamide. The ovarian and plasma levels of 17 beta-estradiol were not affected by treatment with the antiandrogen. The present data show that treatment of intact adult female rats with the pure antiandrogen Flutamide has no effect on the estrous cycle, with no significant change in the plasma concentration of the most important estrogenic compound in the rat, namely, 17 beta-estradiol. The present observation of minor endocrine effects of Flutamide in the intact adult female rat supports clinical trials on the use of this antiandrogen, a potential drug of choice for the treatment of hirsutism, acne and alopecia in women.

17-alpha-Hydroxyprogesterone↗
PubMed1985

Presence of C-19 steroids in mammary Shionogi carcinoma (SC 115) in castrated mice.

Intact and castrated male DD/S mice were inoculated with androgen-dependent cells (SC 115). All intact animals developed tumors after Day 12 of inoculation; however, six of seven castrated animals presented tumors 48 days postinoculation. The levels of steroids in both tumors were then examined. In castrated mice, dehydroepiandrosterone and androst-5-ene-3 beta, 17 beta-diol levels were diminished by 30% and 70%, respectively, while the amounts of testosterone and androstenedione were reduced by more than 90%. Our data also demonstrate that androstane-3 alpha, 17 beta-diol and androstane-3 beta, 17 beta-diol were decreased to 60% and dihydrotestosterone decreased to 6% of their normal value, respectively. This latter level (0.48 nM) was sufficient to still effect a potent androgenic response in the tumor. Besides, a highly significant correlation was found in these tumors between various C-19 steroids (dehydroepiandrosterone and androstane-3 alpha, 17 beta-diol, r = 0.97, P less than 0.01), suggesting a possible conversion of C-19 precursors into potent androgens in the tumors. Determination of the plasma steroid levels in the castrated animals clearly confirmed that potent androgenic steroids and precursors were still in the circulation 3 days after castration. It thus appears that C-19 steroids from adrenal origin may be also involved in "independent" tumor growth.

Animals↗
PubMed1982

Combined long-term treatment with an LHRH agonist and a pure antiandrogen blocks androgenic influence in the rat.

Daily administration for 5 months of the potent LHRH agonist (D-Ser(TBU)6, des-Gly-NH2(10)) LHRH ethylamide (250 ng) in combination with the pure antiandrogen RU23908 (5 mg) to adult male rats causes a marked inhibition of ventral prostate and seminal vesicle weight to 9% and 15% of control, respectively. At the doses used, owing to readjustments of the pituitary-testicular axis, neither treatment alone has an effect on prostate weight and exerts only minimal inhibitory effects on seminal vesicle weight. Whereas treatment with the LHRH agonist alone markedly inhibits testicular LH and PRL receptor levels, the antiandrogen alone stimulates the concentration of the two receptors and reverses the inhibitory effect of the LHRH agonist treatment on LH receptors. Treatment with the LHRH agonist decreases plasma PRL levels, whereas the antiandrogen increases the concentration of circulating LH and FSH by 250%. Treatment with the LHRH agonist decreases the concentration of testosterone and its precursors of the delta 4-pathway while stimulating 5 alpha-reductase activity in both the absence and presence of simultaneous treatment with the antiandrogen. The present data show that blockage of the delta 4-steroidogenic pathway induced by treatment with an LHRH agonist prevents the escape phenomenon observed during long-term treatment with a pure antiandrogen, and permits maximal inhibitory effects of the two treatments on secondary sex organ weight. Such combined treatment with an LHRH agonist (to block androgen formation) and an antiandrogen (to neutralize remaining androgens of testicular and adrenal origin) should be the hormonal therapy of choice in prostatic carcinoma.

Androgen Antagonists↗
PubMed1982

Comparative effects of LHRH agonist and ovine LH administration on testicular steroidogenesis in intact adult rat.

In order to better understand the effects of LHRH administration on testicular function in adult rat, we compared the inhibitory effects of LH and LHRH analogue [D-Ser-(TBU)6, des-Gly-NH2(10)]LHRH ethylamide upon testicular steroidogenesis and LH, FSH and prolactin receptor contents. Administration of LH as well as LHRH analogue resulted in a marked decrease of LH receptor levels, accompanied by a blockage at the level of 17-hydroxylase activity. We have been able to demonstrate that multiple LH administration can achieve a testicular desensitization comparable to that observed after LHRH agonist treatment.

Animals↗
PubMed1980

Increased testicular 5 alpha-androstane-3 alpha, 17 beta-diol formation induced by treatment with [D-Ser (TBU) 6, des-Gly-NH2(10)] LHRH ethylamide in the rat.

While the intact male adult rats respond to LH with a predominant increase of testicular and plasma testosterone levels, the response to LH stimulation in animals treated with the LHRH agonist, [D-Ser(TBU) 6, des-Gly-NH2(10)] LHRH ethylamide is characterized by a major production of 5 alpha-androstane-3 alpha, 17 beta-diol. The marked increase of 5 alpha-androstane-3 alpha, 17 beta-diol levels in the presence of a 90% decrease of testosterone concentration strongly suggests that 5 alpha-reductase and 3 alpha-hydroxysteroid oxidoreductase activities are increased during testicular desensitization induced by treatment with the LHRH agonist.

3-Hydroxysteroid Dehydrogenases↗