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At least 19 recordsLinked to original sources

PubMed1978

[Specific role of sex steroids on the pituitary level. Sex steroids and anterior pituitary secretion].

Although sex steroids were known to play a role in the control of LH, FSH, TSH and prolactin secretion, in vivo experiments could not discriminate between hypothalamic and pituitary sites of action. In this study, the specific action of sex steroids at the anterior pituitary level could be achieved using rat adenohypophyseal cells in primary culture. While estrogens stimulated the sensitivity of the LH and FSH responses to LHRH, androgens had differential effects on the secretion of the two gonadotropins: marked inhibition of LH and stimulation of FSH secretion. Progesterone, on the other hand, while having no effect in the absence of estrogens, could reverse the stimulatory effect of estrogens on LH release while it led to a stimulation of FSH secretion. Estrogens and thyroid hormone exert respective stimulatory and inhibitory effects on TSH secretion by a direct action at the pituitary level. These effects appear to be mediated changes of the level of adenohy-pophyseal TRH receptors. A close correlation was observed between the specificity of binding of the dopamine agonist (3H)dihydroergocryptine and the control of prolactin release in cells in culture, thus supporting the physiological importance of the dopamine receptor in the control of prolactin release. The high degree precision of this system permits assessment of activity of not only dopamine agonists and antagonists, but also of compounds having mixed agonist-antagonistic activity. Preincubation of anterior pituitary cells with 17beta-estradiol not only stimulated basal and TRH-induced prolactin release but, more unexpectedly, led to an almost complete reversal of the inhibitory effect of dopamine agonists on prolactin secretion. Besides its own interest, the adenohypophyseal cell culture system could well be used as a model system for study of the interaction between estrogens and dopaminergic action.

Androgens↗

PubMed1978

Attenuation of stereotyped behaviour by sex steroids.

Effects of sex steroids, testosterone, progesterone, and estradiol on PEA-induced stereotyped behaviour (SB) has been studied in normal, castrated, and ovariectomised mice. Effects of sex steroids on amphetamine-induced sterotypy and hyperactivity are also described. In castrated and ovariectomised mice B-phenylethylamine (PEA) increased SB. Pretreatment with sex steroids attenuated PEA-induced stereotypy in normal, castrated, and ovarietomised mice. Sex steroid pretreatment significantly inhibited PEA- and amphetamine-induced SB, but failed to alter increased motor activity due to amphetamine or PEA. The possible effect of sec steroids on SB through changes in central neurotransmitters are discussed.

Animals↗

PubMed1978

Sex steroids and sex-hormone binding globulin in males with chronic alcoholism.

Thirty men with chronic alcoholism were studied. Biopsies of the liver and testis were performed in all. Serum concentrations of total and non-protein bound (free) testosterone and oestradiol, dihydrotestosterone and sex-hormone binding globulin (SHBG) were determined. Testosterone and dihydrotestosterone concentrations were normal in most patients, whereas oestradiol and free oestradiol were above normal in approximately 50% of the patients. None of the hormones measured differed significantly between patients with and without cirrhosis. SGBG was significantly higher in men with severely reduced spermatogenesis compared to those with intact germinal epithelium, but there was no difference between men with and without cirrhosis. No relation could be demonstrated between clinical signs of hypogonadism and any of the hormones measured. The results support the view that hormonal and sexual disturbances may occur in chronic alcoholism independent of the presence of liver disease.

Adult↗

PubMed1975

Purification of the sex steroid binding protein from human serum.

The sex steroid binding protein from human pregnancy serum was purified to homogeneity by affinity chromatography and preparative polyacrylamide gel electrophoresis. The selective adsorbants were prepared by coupling [3H]-5alpha-dihydrotestosterone 17beta-hemisuccinate to 3,3'-diaminodipropylamine-agarose, poly(Lys-DLAla)-agarose, and albumin-agarose. The most effective adsorbant purifying for the binding protein was 5alpha-dihydrotestosterone 17beta-hemisuccinyl-3,3'-diaminodipropylamine-agarose. A preparative procedure with 5alpha-dihydrotestosterone 17beta-hemisuccinyl-3,3'-diaminodipropylamine-agarose yielded active material which was further purified by preparative polyacrylamide electrophoresis at pH 9.5. Homogeneity was shown by analytical disc gel electrophoresis at three different pH units. A single radioactive band corresponding to the stained band was shown by incubating with [1,2-3H]-5alpha-dihydrotestosterone prior to electrophoresis. The radioactive peak corresponding to the pure sex steroid binding protein could not be detected when a 100-fold excess of 17beta-estradiol was present in the incubation prior to electrophoresis demonstrating the specific sex steroid binding properties of this protein. The migration of this peak was identical with that obtained when diluted serum was electrophoresed under the same conditions in the presence of [1,2-3H]-5alpha-dihydrotestosterone indicating that no significant changes in the molecular characteristics of the binding protein occurred during the purification procedure. The presence of carbohydrate in the pure protein was shown by the periodic acid-Schiff reagent procedure. Selective adsorbants containing 17beta-estradiol linked at the 3 position were ineffective in retaining sex steroid binding protein activity.

Binding Sites↗

PubMed1979

Patterns of transport and binding of sex steroids.

The seminal plasma-sex steroid binding kinetic was evaluated by measuring the amount of labeled hormone extractable after 5 sec to 100 min of incubation. For testosterone in normal subjects, a peak of binding was reached after 30 sec of incubation. In subjects with severe oligoasthenospermia the kinetic pattern for testosterone was different but similar to the binding kinetic between seminal plasma of normal men and estradiol. The phenomena did not occur with frozen plasma samples.

Estradiol↗

PubMed1978

Interaction of digitalis and spironolactone with human sex steroid receptors.

Spironolactone and digitoxin have previously been shown to interact with cytosol androgen and estrogen receptors, respectively, in the rat. The interaction of digitoxin with human uterine cytosol estrogen binding protein and spironolactone with human prostate and newborn prepuce cytosol dihydrotestosterone (DHT) binding protein has been analyzed in this study. Specific estradiol binding was found only in premenopausal uteri. The dissociation constant for estradiol binding was 0.6--2.3 X 10(-9) M (n - 12). Digitoxin in concentrations varying between 0.5--2.0 X 10(-6) M inhibited specific estradiol binding with a Ki of 2.0--7.3 X 10(-7) M (n = 9). The dissociation constants for DHT and the human androgen cytosol binding protein in prostate and newborn prepuce were 0.27--3.0 X 10(-8) M (n = 12) and 0.6--2.0 X 10(-8) M (n = 5), respectively. Spironolactone at concentrations of 0.3--2.0 X 10(-6) M competitively inhibited this binding with an affinity about one order of magnitude less than that of DHT. Digitoxin and spironolactone did not displace estradiol and DHT, respectively, from testosterone-estrogen binding globulin in male or female plasma. The interaction of digitoxin with the human uterus estrogen binding protein and spironolactone with the human prostate and prepuce androgen binding protein is similar to our previous observations in the rat, and may explain the weak estrogenic effects of digitoxin and spironolactone in man.

Binding, Competitive↗

PubMed1975

The feedback effects of sex steroid hormones on pituitary gonadotropin release in Turner's syndrome and Klinefelter's syndrome.

The present study was designed to elucidate the feedback relationship between the release of pituitary gonadotropins and sex steroid hormones in Turner's syndrome and Klinefelter's syndrome. LH-RH stimulation test was employed to evaluate the effects of sex steroids on the release of gonadotropins. The release of gonadotropins in response to LH-RH as well as in baseline level was suppressed after the treatment with estrogen (mestranol 0.08 mg/day) for 10 days, followed by the treatment of the same period with estrogen (mestranol 0.08 mg/day) and progesterone (chlormadinone acetate 2.0 mg/day) in combination in both syndromes. The inhibitory effect of the combined treatment was greater than that of the treatment with estrogen alone. Administration of testosterone propionate (25 mg/day) for 3 days resulted in suppression of the release of both gonadotropins in baseline level and in response to LH-RH in both syndromes, but the suppressive effect appeared to be less complete as compared with that of estrogen or estrogen-progesterone. It was thus verified that the feedback interaction between the pituitary gonadotropin release and sex steroids such as estrogen, estrogen-progesterone or testosterone was operative in the same fashion in the patients with Turner's syndrome and Klinefelter's syndrome.

Adolescent↗

PubMed1975

Sex steroids influence LH-RH-receptor interaction.

Intact male rats (I) and rats 30 days after orchidectomy (OR) were treated in vivo with a single dose of 1.5 or 0.5 mg testosterone propionate (TP), 22.5 or 7.5 mug estradiol benzoate (EB) and a mixture of TP plus EB, respectively. The release of LH and FSH from anterior pituitaries of steroid hormone pretreated animals induced by the administration of LH-RH was studied in vitro. LH-RH stimulated FSH release from pituitaries of I and OR was inhibited by higher doses of EB or a mixture of EB plus TP. On the other hand, EB and combination of EB plus TP stimulated LH release in I, whereas EB and TP inhibited LH-RH induced release of LH in OR. At the lower dose levels no inhibition of LH-RH stimulated FSH release from pituitaries of steroid pretreated I or OR animals occured. LH-RH induced LH release was only observed at thise dose level in I pretreated with TP and OR pretreated with EB. On the other hand, pretreatment of ovariectomized rats (OV) with sex steroids (5 mug 17 beta-estradiol, 3 mg progesterone, and mixture of 5 mug 17 beta-estradiol and 3 mg progesterone, resp., each injected through 6 days) resulted in restoration of LH-RH induced FSH release lost 30 days after ovariectomy. Furthermore, LH-RH induced release of LH and FSH from male rat pituitaries at different times after orc dectomy exhibited a pattern from that recorded for ovariectomized animals. [125I] LH-RH binding assays with anterior pituitary plasma membrane fractions isolated from I revealed two binding sites with apparent affinity constants of 4.3 x 10(-9) M and 2.2 x 10(-8) M, respectively. The low affinity binding site is lost upon orchidectomy. Scatchard plot analyses of binding data obtained for LH-RH reaction with plasma membrane fractions isolated from anterior pituitaries of OR pretreated with sex steroids showed that the second binding site could be regenerated by treatment with the low dose of TP. From the present experiments it is concluded that: 1. LH-RH induced gonadotropin release is affected by sex steroids at the pituitary plasma membrane level. 2. One hypothalamic hormone may well specifically control LH and FSH release. 3. Mechanisms controlling LH-RH induced gonadotropin release are different in the male and female.

Animals↗

PubMed1977

[Changes in adrenal gland and thymus induced by sex steroid administration in newborn rats (author's transl)].

Testosterone, dehydroepiandrosterone (DHEA), progesterone, estradiol-17beta, estrone, estriol, 2-hydroxyestradiol-17beta, 2-hydroxyestriol, deoxyestrone and diethylstilbestrol were injected s.c. in a dose of 0.5 mg each into newborn rats on the first day of life, and changes in the adrenal gland, thymus and spleen were examined 3 days later. Increase in the body weight during the 3 days was less in rats treated with DHEA, 2-hydroxyestriol and deoxyestrone, as compared with that in controls. Development of the thymus was significantly impaired in rats injected with various kinds of sex steroids, except progesterone and diethylstilbestrol. Reduction of the spleen weight by sex steroid treatment was not marked. The weight of adrenal gland decreased in rats injected with DHEA and progesterone, while the weight increased in those given estrone and diethylstilbestrol. Estrogens, particularly estriol, induced a marked increase in adrenal corticosterone content, while 2-hydroxyestriol caused only slight elevation and 2-hydroxyestradiol and deoxyestrone had no influence on the content. Suppressive effect of cortisol on the adrenal gland of newborn rats was slightly, but significantly, lessened by estriol treatment. From the results, physiological role of estriol and DHEA in adrenal secretion was discussed.

Adrenal Glands↗

PubMed1978

[Modulation of the pituitary response to LH-RH by synthetic sex steroids (author's transl)].

This study was planned in order to investigate the response of the pituitary gonadotropin secretion to the luteinizing hormone-releasing hormone (LH-RH) in each menstrual phase (early follicular, late follicular, luteal) of women with regular menstrual cycles, and the effect of synthetic sex steroids on the response of the pituitary to LH-RH, as compared with the response in the late follicular phase. A dose of 200microgram of LH-RH was administered intramuscularly in the early follicular, and luteal phase of regular menstrual cycles. Three groups of 35 normal women administered 3 kinds of sex steroids were also examined on the 8th to 10th day after medication, except for a long-term administration group of norethindrone. The first group was a mestranol group with two subgroups given a daily administration of 20microgram and 40microgram. The second was a norethindrone group, in which one was a short-term group given a daily administration of 5mg, and another was a long-term group given a daily administration of 10mg to 20mg for more than 150 days. The third was a chlormadinone acetate group given a daily administration of 2mg. Blood samples were obtained before the injection of LH-RH at 15, 30, 60, 90, 120, 180 minutes and 24 hours after the injection. Their sera were separated and frozen at -20 degrees C until assayed. Serum LH and FSH concentrations in each experimental group were used as the standard preparation and expressed as mIU/ml of serum. The results were as follows: 1) Serum LH and FSH responsiveness to LH-RH in women with regular menstrual cycles were greater with regard to late folicular, luteal and early follicular phases, respectively, except for a percent increase of serum LH. 2) The serum LH level in response to the LH-RH injection in the early follicular and luteal phases of the cycle showed a biphasic pattern of elevation characterized by the first pool, releasable LH; and the second pool, newly synthesized and stored LH in the pituitary. The biphasic pattern of serum FSH was not confirmed in this experiment. 3) Sham disappearance of biphasic pattern of serum LH release in the late follicular phase was attributed to a shifting of LH form the 2nd pool to the 1st pool due to an increase of the endogenous estrogen. 4) The capacity of the pituitary FSH synthesis and storage showed a slight increase in the late follicular phase, which was supposed to be enhanced by estrogen. 5) The serum LH peak in the mestranol group was observed at 120 minutes after the LH-RH injection, which was significantly elevated in the group given a daily administration of 40microgram, as compared with the control group. The LH concentration occupied in a definite volume tended to be reduced in the first pool after the LH-RH injection in the mestranol group and didnt change in the second pool after the injection, as compared with the control group...

Estradiol Congeners↗

PubMed1978

Characterization of the sex steroid binding protein of human pregnancy serum. Improvements in the purification procedure.

The sex steroid binding protein (SBP) of human pregnancy serum was purified to homogeneity by the sequential use of ammonium sulfate precipitation, affinity chromatography on 5alpha-dihydrotestosterone-17beta-succinyldiaminoethyl-(1,4-butanediol diglycidyl ether)-agarose, and preparative polyacrylamide gel electrophoresis. The yield of pure SBP was improved from 5% as originally reported [Mickelson, K. E., and Petra, P. H. (1975), Biochemistry 14, 957] to 34%. Homogeneity of SBP was shown by equilibrium sedimentation ultracentrifugation in 6 M guanidine hydrochloride containing 0.1 M mercaptoethanol which yields a minimum molecular weight of 36 335 +/- 525. The protein is also homogeneous when examined by gel electrophoresis in the presence of sodium dodecyl sulfate. A value of 52 000 for the molecular weight is obtained by this method. SBP partially purified from Cohn fraction IV has also a molecular weight of 52 000 by gel electrophoresis in the presence of sodium dodecyl sulfate; that fraction is contaminated with another protein of molecular weight 90 000 which must be removed to obtain homogeneous SBP. The amino acid composition of SBP isolated from pregnancy serum is presented.

Amino Acids↗

PubMedDate not supplied

[Role of the adrenal glands and the testes in the formation of the sex steroid pool in the peripheral blood of male monkeys].

A study was made of formation of the pool of sex steroid hormones and their precursors in the blood plasma of male Paio hamadryas. Cannulation and simultaneous recovery of the blood from the adrenal, testicular, left iliac veins and the aorta were carried out under nembutal anesthesia. Thirteen steroid hormones and their precursors were determined by the radioimmunological method in all the blood portions. Steroid function was tested on columns with celite. Pregnenolone, 17alpha-oxypregnenolone, and 17alpha-oxyprogesterone were secreted chiefly by the adrenal glands. Dihydroepiandrosterone was produced by the adrenal glands and utilized by the testes. Androstendion and dihydrotestosterone were mostly of adrenal, and testosterone--testicular origin. Estron is secreted by the adrenal glands only, whereas estradiol is produced by the testes in larger quantities than by the adrenal glands. The sulfate forms of pregnenolone and dihydroepiandrosterone are produced chiefly by the adrenal glands.

Adrenal Glands↗

PubMed2024

Phthalates and sex steroid hormones across the perimenopausal period: A longitudinal analysis of the Midlife Women's Health Study.

BACKGROUND: The menopausal transition involves significant sex hormone changes. Environmental chemicals, such as urinary phthalate metabolites, are associated with sex hormone levels in cross-sectional studies. Few studies have assessed longitudinal associations between urinary phthalate metabolite concentrations and sex hormone levels during menopausal transition. METHODS: Pre- and perimenopausal women from the Midlife Women's Health Study (MWHS) (n = 751) contributed data at up to 4 annual study visits. We quantified 9 individual urinary phthalate metabolites and 5 summary measures (e.g., phthalates in plastics (∑Plastic)), using pooled annual urine samples. We measured serum estradiol, testosterone, and progesterone collected at each study visit, unrelated to menstrual cycling. Linear mixed-effects models and hierarchical Bayesian kernel machine regression analyses evaluated adjusted associations between individual and phthalate mixtures with sex steroid hormones longitudinally. RESULTS: We observed associations between increased concentrations of certain phthalate metabolites and lower testosterone and higher sub-ovulatory progesterone levels, e.g., doubling of monoethyl phthalate (MEP), monobenzyl phthalate (MBzP), di-2-ethylhexyl phthalate (∑DEHP) metabolites, ∑Plastic, and ∑Phthalates concentrations were associated with lower testosterone (e.g., for ∑DEHP: -4.51%; 95% CI: -6.72%, -2.26%). For each doubling of MEP, certain DEHP metabolites, and summary measures, we observed higher mean sub-ovulatory progesterone (e.g., ∑AA (metabolites with anti-androgenic activity): 6.88%; 95% CI: 1.94%, 12.1%). Higher levels of the overall time-varying phthalate mixture were associated with lower estradiol and higher progesterone levels, especially for 2nd year exposures. CONCLUSIONS: Phthalates were longitudinally associated with sex hormone levels during the menopausal transition. Future research should assess such associations and potential health impacts during this understudied period.

Humans↗

PubMed1979

Is there an embryo-fetal exogenous sex steroid exposure syndrome (EFESSES)?

A survey of all outpatient cases referred for genetic counseling during a 10-month period has revealed a history of preconceptional and early gestational exposure to maternally administerd sex hormones in 16 of 91 instances. Particular interest was aroused by 9 of these 16 cases, all of whom were children with dysmorphic features, no cytogenetic anomalies by Giemsa banding studies, and no recognizable clinical diagnosis. Similarities among them were striking and consisted of varying combinations of the following features: moderate growth retardation; mild to severe mental retardation; facial elongation with frontal bossing; primary telecanthus and downward-slanting palpebral fissures; broad, flat, nose bridge and pug nose; pouting lower lip and blunt, square chin; umbilical eversion; deep sacral pit; and, in males, moderate to severe external genital anomalies ranging from mild hypospadias to genital ambiguity. This may suggest the existence of an embryo-fetal exogenous sex steroid exposure syndrome.

Abnormalities, Drug-Induced↗

PubMed1979

Sex steroid control of intermale fighting in mice.

The data presented here are based on over 700 mice and employed over 13,000 injections. The results obtained provide good evidence that the influences of sex steroids on fighting motivation in aggressive mice are discrete from the somatic influences of these hormones. Further, it seems possible that some of the effects of naturally occurring endogenous androgens in the mouse are consequent upon local neural aromatization of these compounds to estrogenic metabolites, before they exert an influence on aggressive motivation. It seems possible that this is a physiological effect as well as a consequence of pharmacological influence, as the doses of steroid employed in this present study are quite low. However, this model of hormone action cannot be the entire story, as 5 alpha DHT is behaviorally effective even though its A ring cannot be aromatized. Aggressive mice seem useful behavioral models for these effects. These studies indicate some of the likely sources of variability in the literature, as well as providing a number of considerations for clinical behavior therapy. They also indicate some of the features of steroid hormones (such as an aromatized A ring; the presence of a hydroxyl group at position 19; the influence of alpha hydroxyl groups, etc.) which may change the behavioral and somatic influences of these compounds.

Aggression↗

PubMed1977

Sex steroid production by the human fetus: its role in morphogenesis and control by gonadotropins.

Normal male genital differentiation requires fetal testicular secretion of both testosterone and the nonsteroidal müllerian-inhibitory factor. It appears that secretion of testosterone, at least during the critical period of differentiation, occurs in response to stimulation by CG, although pituitary LG may influence Leydig cell function in later fetal life. To date, there is no evidence to support a similar endocrine function for the fetal ovary in female genital differentiation. In both sexes normal fetal pituitary gonadotropin secretion appears to be required for maturation of the germ cells and related elements. The pattern of FSH and LH secretion in the fetus reflects gradual maturation of a functional hypothalamo-pituitary unit responsive to feedback inhibition by sex steroids. The higher levels of gonadotropins in female fetuses from from 12--20 weeks suggest either that this maturation occurs earlier in males than in females, or, more probably, that feedback recognition of androgens is established before gestation reflects development of an estrogen-mediated feedback mechanism, and in addition the possible influence that hormones, such as prolactin or placental estradiol, may have on testicular steroidogenesis.

Androgens↗

PubMed1976

Plasma adrenal and gonadal sex steroids in human pubertal development.

Plasma free dehydroepiandrosterone (DHA), androstenedione (delta), testosterone (T), dihydrotestosterone (DHT), estrone (E1), and estradiol (E2) were measured by radioimmunoassay in 55 boys and 54 girls 3.5 to 16.3 years of age. Plasma DHA increased significantly between 6 and 8 years of age in girls and between 8 and 10 years of age in boys. A further significant increase was noted between 10 and 12 years of age in both sexes. Delta rose significantly between 8 and 10 years of age in girls and between 10 and 12 years in boys. In contrast, no significant increase in T, DHT, or E1, was noted prior to 12 years of age in both sexes. However, E2 showed a significant increase between 10 and 12 years of age in girls. This early rise in the course of pubertal development of the two sex steroids predominantly of adrenal origin, DHA and delta, and its occurence 1 to 2 years earlier in girls than in boys, as does puberty itself, suggest a possible role for these steroids in the mechanisms involved in triggering the hypothalamic-pituitary-gonadal axis at puberty.

Adolescent↗

PubMed1977

Steroid sex hormones and prolactin in postmenopausal women with generalized mammary carcinoma during prolonged dexamethasone treatment.

The endocrine response to prolonged dexamethasone treatment was investigated in six postmenopausal women with generalized mammary carcinoma. Plasma cortisol levels decreased rapidly and became undetectable whereas significant concentrations of plasma dehydroepiandrosterone and androstenedione persisted throughout the study, even in two ovariectomized patients, indicating a certain degree of autonomy or a greater resistance of adrenal 'androgens' to the inhibition of ACTH secretion. Except in the ovariectomized patients, plasma testosterone did not fall significantly whereas the plasma oestrogens tended progressively towards undetectable concentrations. A similar response was found in six normal postmenopausal women although the disappearance of their oestrogens was relatively rapid. This indicates that much of the testosterone present after the menopause could still be produced by the ovaries whereas the ovarian production of oestrogens becomes negligible. The delayed disappearance of oestrogens in the patients with mammary carcinoma indicates that the persisting adrenal 'androgens' remained efficient precursors of oestrogen synthesis within the peripheral tissues and presumably within the mammary tumour itself. Plasma dihydrotestosterone behaved like the plasma oestrogens. Despite the fall in plasma oestrogens, plasma gonadotrophins did not increase further but plasma prolactin rose progressively. The persistance of steroid sex hormones and the rise of plasma prolactin might explain the poor response to dexamethasone treatment in mammary carcinoma.

Aged↗