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PubMedDate not supplied

17beta-estradiol regulation of human growth hormone (hGH), insulin-like growth factor-I (IGF-I) and insulin-like growth factor binding protein-3 (IGFBP-3) axis in hypoestrogenic, hypergonadotropic women.

OBJECTIVE: Ovarian hormonal function may be as important contributing factor to hGH-IGF-I-IGFBP-3 axis as age. AIM: To examine plasma hGH, IGF-1 and IGFBP-3 levels in women with premature ovarian failure compared to healthy normal controls and postmenopausal ones. PATIENTS: Group A-15 women with premature ovarian failure (POF) (mean: age 38.9+/-5.2 years, FSH 101.4+/-29.0 IU/l; 17beta-estradiol 22.5+/-14.6 ng/l). Group B consisted of 15 menopausal women (mean: age 54.7+/-2.7 years; FSH 81.9+/-32.1 IU/l; 17beta-estradiol 17.1+/- 8.0 ng/l). Group C - controls - 15 normally menstruating women (mean: age 37.1+/-9.0 years; FSH 6.2+/-1.0 IU/l; 17beta-estradiol 144.8+/-117.1 ng/l). METHODS: Body mass and BMI were measured. Basic fasting plasma hGH, IGF-I, IGFBP-3, insulin, testosterone and LH as well as prolactin (PRL), FSH and estradiol were assessed by RIA kits. Statistical analysis. Shapiro-Wilk test, Mann-Whitney u-test, Spearman rang correlation coefficient, stepwise multiple regression. RESULTS: Mean serum IGF-I level was the lowest (p<0.005) in group B (172.0+/-54.6 microg/l) and the highest in group C (273.6+/-109.0 microg/l). The mean plasma IGF-I level in group A was similar (NS) (208.3+/-66.5 microg/l) to that found in group B and lower (p<0.02) compared with that in group C. The lowest (p<0.005) serum IGFBP-3 level was found in group B (3.1+/-0.7 microg/l) compared to group C (4.4+/-0.3 microg/l). The mean plasma IGFBP-3 level (3.1+/-1.0 microg/l) in group A was lower than in group C (p<0.005) but identical as in group B. No statistically significant differences between groups were observed in mean hGH levels. Women in group A and C were younger (p<0.001) than those in group B. The lowest mean estradiol level was found in groups A and B. The highest was in group C (p<0.001). Mean plasma LH and FSH levels were higher (p<0.001) in groups A and B vs group C. In group C there were links between IGF-I and age (r=-0.60; p=0.014) The IGF-I/age relation disappeared in the groups A and B (rA=-0.26; rB=0.10; NS). The same regards IGFBP-3/ age link (rA=-0.44, NS; rB=0,31;NS). Estradiol level was related to hGH levels in group C (r=-0.54; p<0.05). In none of groups hGH/IGF-1 as well as IGFBP-3/hGH relations were found. Prolactin accounted for 69% of the variance in IGF-I level in the group B (p=0.003) and for 24% in group A (NS). Testosterone accounted for 88% (p=0.004) of the variance in IGF-I level in group B and IGFBP-3 was responsible for 86% (p=0.038) of the variance in IGF-I level in group C. Again IGFBP-3 was responsible for 47% (p=0.023) in group A and for 49% (p=0.04) in group B of the hGH variance. CONCLUSIONS: 17b-estradiol may be as important contributor to insulin-like growth factor-I (IGF-I) plasma level as age in hypoestrogenic, hypogonadotropic women.

Adult↗
PubMed1991

Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on 17 beta-estradiol-induced glucose metabolism in MCF-7 human breast cancer cells: 13C nuclear magnetic resonance spectroscopy studies.

The effects of 17 beta-estradiol, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), and their combination on the metabolism of [1-13C] glucose were determined in cell suspensions of wild-type MCF-7 human breast cancer cells, by 13C NMR spectroscopy. Preliminary studies showed that, during the 7-hr duration of the NMR experiment, the cells maintained their viability and their aryl hydrocarbon responsiveness. Lactate was the major glucose metabolite detected in these studies, and the rate of lactate formation in the untreated (control) and 17 beta-estradiol (10(-9) M)-treated cells was 60 and 86 fmol/cell/hr, respectively; this represented a 40% increase in lactate formation in the cells treated with 17 beta-estradiol; comparable results were observed for the percentage of glucose converted into lactate. In contrast, TCDD (10(-9) M) did not significantly alter the rate of glucose metabolism or lactate formation. Co-treatment of the cells with 17 beta-estradiol (10(-9) M) plus TCDD (10(-8) to 10(-10) M) showed that TCDD completely inhibited the 17 beta-estradiol-induced metabolism of [13C] glucose to lactate in MCF-7 cells. In contrast, 2,8-dichlorodibenzo-p-dioxin (10(-8) M), a weak aryl hydrocarbon receptor agonist, did not inhibit estrogen-induced glucose-to-lactate metabolism in MCF-7 cells. In addition, it was shown that TCDD caused a significant decrease in 17 beta-estradiol-induced lactate formation within 1 hr after treatment, whereas the induction of monooxygenase activity was not observed until 3 hr after exposure of the cells to TCDD. These data indicate that TCDD-induced 17 beta-estradiol metabolism is not related to the decrease in the rate of conversion of glucose to lactate. These results further define the antiestrogenic responses elicited by TCDD and show that 13C NMR spectroscopy provides a unique method for measuring, in real time, the effects of TCDD on specific metabolic pathways.

Breast Neoplasms↗
PubMed1991

Relationship of selected body composition and training variables to 17 B-estradiol in eumenorrheic runners.

Although the relationships among body composition, training, and physical characteristics and 17 B-estradiol (estradiol) have been described in active amenorrheic women, little is known about these relationships in eumenorrheic women. This study examined the relationship between selected body composition and training variables, physical characteristics, maximal oxygen consumption (VO2max), luteinizing hormone (LH) and estradiol in eumenorrheic runners. Fifteen women (25.8 +/- 0.8 years) running 19.8 +/- 1.8 miles per week were studied during the midluteal phase of the menstrual cycle. Estradiol and LH were determined by radioimmunoassay. Body composition was measured by hydrostatic weighing. Age, Ponderal Index, and menstrual cycle length (days) were inversely related to estradiol (r = -0.56, r = -0.55, r = -0.52, respectively, p less than 0.05). A significant relationship (R2 = 0.91; p less than 0.05) was found among age, menstrual cycle length, LH (mIU/ml), VO2max (ml/kg/min), weight training (hr/wk), miles run per week, height (cm), additional aerobic training (hr/wk), relative body fat (%), and Ponderal Index and estradiol (pg/ml). These data suggest the midluteal concentration of estradiol in moderately trained eumenorrheic runners is the result of a complex interaction of many factors.

Adult↗
PubMed1991

Membrane-mediated effects of the steroid 17-alpha-estradiol on adrenal catecholamine release.

The effects of 17-alpha-estradiol on the secretion of catecholamines from the perfused bovine and cat adrenal gland and bovine chromaffin cells in culture elicited by dimethylphenylpiperazinium (DMPP), methacholine and high potassium were studied. In perfused cat adrenal glands, secretion of catecholamines evoked by pulses of DMPP (1 microM for 30 sec) was decreased by 17-alpha-estradiol at concentrations of 1 and 10 microM by 50 and 80%, respectively. However, secretion evoked by pulses of methacholine (3 microM for 30 sec) was not affected by 1 microM of 17-alpha-estradiol and was affected to a variable extent by 10 microM 17-alpha-estradiol. Catecholamine secretion evoked by higher concentrations of methacholine (100 microM for 60 sec) was reduced by 50% by 10 microM 17-alpha-estradiol. 17-alpha-Estradiol decreased secretion evoked by pulses of 120 mM K+ for 10 sec to a similar extent in the perfused bovine and cat adrenal gland. The 45Ca++ uptake into bovine chromaffin cells in culture stimulated by DMPP (100 microM for 10 sec) or high K+ (59 mM for 10 sec) was almost inhibited completely by 100 microM 17-alpha-estradiol. The rapid action precludes a classical genomic mechanism and suggests effects at the cell membrane.

Adrenal Glands↗
PubMed1989

[Effects of testosterone and estradiol-17 beta on the secretory granules of rat submandibular gland].

The effects of testosterone and estradiol-17 beta on the protein components, amino acid compositions and trypsin-like protease activities in the secretory granules of granular duct cells of rat submandibular glands were assayed. Male and female adult rats were divided into 4 groups, non treatment (control), castrated, testosterone injected and estradiol-17 beta injected groups. The castrated rats were received 5 injections of 5 mg/kg testosterone or 500 micrograms/kg estradiol-17 beta every other day 3 weeks after the castration. The secretory granules of submandibular gland obtained from each group were prepared using centrifugal fractionation with sucrose step gradient. The protein components of secretory granule were separated by 5-15% SDS-PAGE, and the SDS-PAGE revealed the characteristic proteins of MW 39,000 in male and MW 37,000 in female. The MW 39,000 and the MW 37,000 protein was disappeared by testectomy and ovaryectomy, respectively. The MW 39,000 protein was reappeared in the castrated male rat treated by testosterone and shown in castrated female rat treated by the same steroid. Similary the MW 37,000 protein was found in the castrated male and female rats treated by estradiol-17 beta. From the results of amino acid composition analysis, abundant Asp, Ser, Glu and Gly were revealed in the MW 39,000 protein and MW 37,000 protein. Trypsin-like protease activity located in secretory granule was reduced by castration in both male and female, however, the enzyme activities were elevated by testosterone or estradiol-17 beta injection, revealing rather higher activities than control. It was demonstrated that the secretory granule of rat submandibular gland contained the testosterone dependent protein having a MW of 39,000 and the estradiol-17 beta dependent protein having a MW of 37,000 and that the trypsin-like protease activities in the granules were sensitive to both testosterone and estradiol-17 beta.

Animals↗
PubMed1989

The oxidative metabolism of estradiol: inhibition by cimetidine.

Cimetidine, a histamine H2 antagonist, is known to interfere with the metabolism of exogenous drugs by binding to cytochrome P450. We examined the possibility that cimetidine might also inhibit the cytochrome P450-dependent biotransformation of endogenous compounds such as steroid hormones. Utilizing a radiometric assay and normal male volunteers, the acute effect of intravenous cimetidine (300 mg loading dose followed by 50 mg/hr) was determined. The extent of 2-hydroxylation of estradiol was reduced by 25% from 29.6 +/- 4.4% (mean +/- SEM) before, to 22.9 +/- 4.0% during cimetidine infusion (n = 8; p less than 0.0005). Following oral cimetidine (800 mg b.i.d.) for 2 wk, estradiol 2-hydroxylation was decreased by 40% from 31.7 +/- 2.3% to 19.7 +/- 2.4% (n = 9; p less than 0.0001) but 16 alpha-hydroxylation of estradiol was unaffected. Concomitantly, the urinary excretion of 2-hydroxyestrone was decreased by 25% (p less than 0.002) and the serum estradiol concentration was increased by 20% (p less than 0.04). In contrast, ranitidine, a second generation H2 receptor antagonist, had no effect on estradiol hydroxylation following 150 mg b.i.d. for 2 wk. The inhibition of estradiol 2-hydroxylation and the increase in serum estradiol concentrations caused by cimetidine administration may help to account for the symptoms of hyperestrogenization reported in long-term cimetidine therapy.

Administration, Oral↗
PubMed1989

Serum testosterone and estradiol 17-beta concentrations in 15 dogs with perineal hernia.

Serum testosterone and estradiol 17-beta concentrations, and serum testosterone-to-estradiol ratio were evaluated in 15 dogs (greater than or equal to 5 years old) with perineal hernia (9 sexually intact males and 6 castrated males) and in 9 clinically normal sexually intact male dogs greater than or equal to 5 years old. There was no significant difference in serum testosterone-to-estradiol ratio between sexually intact male dogs with perineal hernia and clinically normal sexually intact male dogs. In castrated dogs with perineal hernia, serum testosterone concentration and testosterone-to-estradiol ratio were significantly (P less than 0.05) lower, compared with those values in sexually intact dogs with perineal hernia and in clinically normal sexually intact male dogs. There was no significant difference in serum estradiol 17-beta concentration among sexually intact male dogs with perineal hernia, castrated dogs with perineal hernia, and clinically normal sexually intact male dogs. Serum testosterone and estradiol 17-beta concentrations in dogs with perineal hernia did not differ from those values in clinically normal male dogs of the same age. Castration cannot be recommended for the treatment of perineal hernia unless a castration-responsive contributing factor such as prostatomegaly is identified, unless the pelvic diaphragm of dogs with perineal hernia has high sensitivity to normal or low serum testosterone and estradiol 17-beta concentrations, or unless there is documentation that other androgens and/or estrogens are involved.

Animals↗
PubMed1988

[Translocation of protein kinase C from cytosol into cell membranes after treatment with estradiol and enzyme activation in target cells].

The effect of 17 beta-estradiol on protein kinase C in target cells was studied. It was shown that 10-15 min after injection of ovariectomized animals with estradiol (10 micrograms intraperitoneally) protein kinase C is translocated from the cytosol into the cell membranes of estradiol-dependent mammary gland tumours. A similar effect of estradiol on protein kinase C is observed in uterine tissue. On the contrast, in hormone-independent rat mammary gland tumours estradiol causes no redistribution of protein kinase C between the cytosol and cell membranes. No protein kinase C accumulation in the membranes of hormone-dependent mammary gland tumours is observed 30 min after estradiol injection. However, this period is characterized by the appearance of protein kinase whose activity is not stimulated by Ca2+ or phosphatidylserine and which is eluted from DEAE-cellulose with 0.2 M NaCl. This protein kinase presumably corresponds to the M-fragment, i.e., the catalytic part of protein kinase C formed as a result of protein kinase C proteolysis on the membranes. It seems likely that estradiol, similar to growth factor peptides, realizes its stimulating effect on cell division primarily at the expense of coupling of its membrane receptors with the protein kinase C activation system.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1988

Effect of 17 beta-estradiol on the growth of estrogen receptor-positive human melanoma in vitro and in athymic mice.

Physiochemical properties of an estrogen binding protein were characterized in three human melanoma cell lines, UISO-MEL-1, UISO-MEL-2, and UISO-MEL-4. Estrogen binding to melanoma cytosol was saturable, specific for estrogens, and represented by a single class of high-affinity, limited-capacity binding sites (Kd 5.5 x 10(-10) M, 2.7 +/- 0.5 fmol/mg of cytosol protein, UISO-MEL-2; 2.2 x 10(-10) M, 7.8 +/- 3.3, UISO-MEL-4) (SEM). UISO-MEL-1 cytosols did not bind estradiol. The binding protein in UISO-MEL-2 and -4 sedimented at 8.5S and 9.2S, respectively, in the presence of 10 mM sodium molybdate. Solid-phase radioimmunoassay with a monoclonal antibody specific for human estrogen receptor (H222 sp lambda) showed good correlation (r = 0.84) with a hydroxyapatite biochemical assay of identical melanoma cytosols. Exposure of UISO-MEL-2 to estradiol produced a time- and temperature-dependent increase in total nuclear receptor for estrogen in vitro. Estradiol treatment of athymic mice also significantly increased cytosol progesterone receptor content in UISO-MEL-2 and UISO-MEL-4 xenografts. Estradiol had no effect on the plating efficiency or growth of any melanoma cell line or normal melanocytes in vitro. Tamoxifen also had no effect on melanoma growth in vitro. In contrast, chronic exposure of athymic mice carrying estrogen receptor-positive UISO-MEL-2 to estradiol resulted in a sex-dependent increase in tumor latency and overall inhibition of tumor growth. Taken together, these observations suggest that a subset of human melanomas contains limited amounts of an estrogen binding protein similar to that observed in other estrogen-responsive tissues. The lack of effect of estradiol on melanocyte and melanoma growth in vitro, coupled with a decrease in tumor growth in athymic mice, suggests that, while inhibition may be receptor mediated, possible indirect actions of estradiol must also be considered.

Animals↗
PubMed1987

Specific IgA and IgG antibodies in the secretions of the female reproductive tract: effects of immunization and estradiol on expression of this response in vivo.

Uterine and vaginal secretions collected from intact adult female rats were analyzed to determine whether immunization at sites distal to the reproductive tract had any effect on the presence of specific IgA and IgG antibodies in genital tract secretions. Peyer's patch and i.p. immunization and boost with sheep red blood cells (SRBC) stimulated the appearance of specific IgA antibodies in uterine and vaginal secretions of uterine-ligated animals. IgG antibodies were also induced in uterine but not in vaginal secretions. In contrast, subcutaneous immunization and boost elicited a weak IgA uterine and IgG vaginal response. To establish the role of estradiol in regulating the presence of specific antibodies in the female genital tract, ovariectomized rats received primary and/or secondary Peyer's patch immunizations with hormone treatment. Administration of estradiol daily for 3 days before sacrifice resulted in a significant accumulation of IgA and IgG antibodies to SRBC in uterine secretions. In the absence of estradiol, antibody content was negligible. Vaginal antibody levels were also clearly influenced by estradiol. In contrast to the uterus, however, specific IgA and IgG antibodies were present in the vaginal secretions of saline-injected immunized animals and were markedly inhibited in animals treated with estradiol. These results indicate that antibodies in genital tract secretions can be induced by immunization of the Peyer's patches and that their presence in uterine secretions is clearly dependent on estradiol. Further, they indicate that gut-derived specific antibodies enter the vagina in the absence of hormone stimulation and that estradiol exerts an inhibitory effect on their presence in vaginal secretions.

Animals↗
PubMed1985

The uptake of [3H]estradiol by mouse preimplantation embryos in vitro.

Mouse blastocysts collected on day 4 were cultured for 20 hours in media containing various concentrations of [3H]estradiol with/without 10(-6) M unlabelled estradiol. There was a significant reduction in the radioactivity of embryos cultured at 4 degrees C compared with that of embryos cultured at 37 degrees C. The radioactivity of embryos kept in the washing solution after washing was slight lower but showed no significant difference when it was compared with that of embryos not kept in this way. There was no significant difference between the radioactivity of embryos cultured in 2 X 10(-8) M [3H]estradiol and that of embryos cultured in 2 X 10(-8)M [3H]estradiol plus 10(-6)M non-labelled estradiol. Furthermore the radioactivity of embryos incubated in 2.5 X 10(-8)M [3H]estradiol is more than twice that of embryos incubated in 10(-8)M [3H]estradiol. These results demonstrate that preimplantation mouse embryos are capable of uptake and retaining of estrogen and that the mechanism of uptake is neither selective nor receptor mediated.

Animals↗
PubMed1979

[Comparison of the action of an impeded estrogen, frideron, and of estradiol on the seminal vesicles and on the weight of the testicles and accessory sex glands in the rat. II].

We have undertaken a comparative study on the effects of estradiol and of an impeded estrogen, zeranol, in the prepubescent Wistar male rat. Both had an inhibitory effect on the secretion of F.S.H. in the spermatogenesis test. Nine injections of estradiol or nine ingestions of zeranol had a restraining effect with a dose of 0.5 microgram of estradiol or of 500 micrograms of zeranol (for 100 g of body weight). With some animals, spermatogenesis is interrupted and the weight of the testicles decreased; the treatment is more active with stronger doses: 2 micrograms of estradiol interrupted spermatogenesis in 10 rats out of 11, 1.000 microgram of zeranol interrupted it in 10 rats out of 13. A weak dose of either estrogen (0.05 microgram of estradiol or 20 micrograms of zeranol) stimulated the growth of the seminal vesicles, the prostate gland and the preputial glands. Strong doses decrease the weight of the preputial glands, and even more the weight of the prostate gland (10 micrograms of estradiol, 1.000 microgram of zeranol). They are ineffective on the seminal vesicles. The effects of 2 micrograms of estradiol on the testicles and the accessory sexual glands are completely inhibited by the simultaneous administration of 2 U.I. of P.M.S. rich in FSH.

Animals↗
PubMed1979

Failure of rotenone to interfere with 17 beta-estradiol action in the rat uterus.

The involvement of rotenone in rat mammary carcinogenesis has been suggested to occur through estrogenic effects. This hypothesis was tested by determining the extent of rotenone inhibition of 17 beta-estradiol binding to the estrogen receptor and of the 17 beta-estradiol-induced uterotrophic response in ovariectomized Sprague-Dawley rats. Estradiol binding to the uterine estrogen receptor in the presence of rotenone was determined by charcoal assay and Scatchard analysis. Additionally, 17 beta-estradiol-receptor interactions were assessed on sucrose density gradients. No inhibition of binding was observed in either assay with ratios of rotenone/17 beta-estradiol in excess of 10,000. Finally, an in vivo approach was used to extend the in vitro data. Silastic capsules containing rotenone or 17 beta-estradiol were implanted in various combinations into eight groups of ovariectomized Sprague-Dawley rats (four rats/group). After five days, uteri were removed and weighed. An analysis of variance revealed that rotenone neither interfered with 17 beta-estradiol-induced uterine weight gain nor displayed any uterotrophic properties by itself. Results from these three procedures demonstrate that rotenone does not act as an estrogen or as an estrogen antagonist. Additionally, there were no other effects attributable to rotenone.

Animals↗
PubMedDate not supplied

[Estradiol reception and induction of DNA-dependent RNA synthesis and adaptive enzymes in the mammary glands of mice].

The content of estradiol receptors in the mammary glands of virgin female mice, and the capacity of this hormone to induce RNA synthesis, hexokinase, pyruvatkinase, and glucose-6-phosphoric dehydrogenase in the glands was studied. H3-estradiol binding to the mammary glands was found to be highly specific: only estradiol, and, to a lesser degree, estron, competed with H2-estradiol for the binding sites, while progesterone and hydrocortisone failed to affect the binding of H3-estradiol. As determined by the method of exchange of the receptor-bound endogenous hormone for the labeled exogenous one, the value of H3-estradiol specific binding was 4.3+/-1.5 10(-15) M/mg protein. Under the influence of estradiol the incorporation of H3-adenine and H3-orotic acid into the RNA of the mammary glands increased by 70%, and activity of the enzymes under study was almost doubled.

Animals↗
PubMed1983

Increase of serotonin receptors in rat uterus induced by estradiol.

[3H]Spiroperidol was used to label uterine membrane-binding sites that have the characteristics expected of serotonergic receptors. The characteristics of specific [3H]spiroperidol binding to the uterine membrane of 17 beta-estradiol-3-benzoate-treated ovariectomized rats were studied. The specific [3H]spiroperidol binding was rapid and reversible, and the half-maximal saturation, taken as the apparent dissociation constant (KD) for [3H]spiroperidol, was 5.16 +/- 0.24 (n = 12) nM [3H]spiroperidol. Scatchard plots of saturation curves of the specific [3H]spiroperidol binding were convex and the Hill coefficient was 2.06 +/- 0.11 (n = 12). Cinanserin, mianserin, metergoline (which are serotonergic antagonists), and serotonin (5-HT) inhibited the [3H]spiroperidol binding with apparent Ki values of 21.2, 14.1, 14.1, and 176.5 microM, respectively. Concentrations of 1 mM sulpiride (a dopaminergic antagonist) and dopamine reduced [3H]spiroperidol binding only 26 and 23%, respectively. 1 mM GTP reduced the potency of 5-HT (10(-6) - 10(-3) M) to displace bound [3H]spiroperidol. The uterine membranes were treated with various enzymes and protein-modifying reagents, and binding studies on the treated uterine membranes showed that protein(s), phospholipids, and N-acetyl-neuraminic acid in uterine membranes were important as specific binding sites of [3H]spiroperidol. Measurement of the specific binding of [3H]spiroperidol to uterine membranes from untreated and estradiol-treated ovariectomized rats showed that estradiol significantly increased the number of specific binding sites of [3H]spiroperidol, but did not change the apparent affinity of specific [3H]spiroperidol binding. Estradiol also did not change the dissociation constant or the number of binding sites for [3H]3-quinuclidinyl benzilate, which binds to muscarinic acetylcholine receptors. These findings suggest that [3H]spiroperidol mainly binds to 5-HT receptors in the uterine membrane of estradiol-treated ovariectomized rats. The finding that administration of estradiol significantly increased the number of [3H]spiroperidol-binding sites is consistent with the specific increase in the contractile response to 5-HT observed in isolated uterus from ovariectomized rats treated with estradiol.

Animals↗
PubMed1984

Morphofunctional modifications associated with the inhibition by estradiol of MtTF4 rat pituitary tumor growth.

The MtTF4 pituitary tumor has been induced in Fischer rats by chronic estrogen administration. Recently, we reported that sustained pharmacological treatment of Fischer rats with 17 beta-estradiol inhibited the growth of the MtTF4 tumor transplanted s.c. The present work describes the associated morphofunctional changes occurring in the tumor during 17 beta-estradiol inhibition. It is shown that a 7-day 17 beta-estradiol treatment resulted in an increase of the surface area of cells, nuclei, nucleoli, Golgi complexes, and rough endoplasmic reticulum and an increase in the number of euchromatin-rich nuclei. Flow cytometry analysis of DNA distribution suggested that estradiol affects the cell progression through the early S phase. The ratio of RNA to DNA increased significantly, reflecting cell hypertrophy. Moreover, there was a significant increase in tumor prolactin concentration and a marked enhancement in the intensity of the immunocyto-chemical reaction with rat prolactin antiserum. On the other hand, cell mitoses were dramatically decreased. These morphofunctional changes indicate that the inhibition of the tumor growth by estradiol is accompanied by an evolution of the tumor cell population towards a more differentiated state. However, it cannot be decided whether 17 beta-estradiol induces a shift from a proliferative state to a differentiated state or whether 17 beta-estradiol treatment results in a selection of a subpopulation of tumor cells that are slow growing and more differentiated.

Animals↗
PubMed1994

[Changes in the weight of the uterus, ovaries and adrenal glands in sexually mature rats treated with estradiol and reserpine].

Immature rats of the Wistar strain were used for the experiments. The treatment was administrated on the 35, 36, 37th day after delivery. The animals were divided into 4 groups. The first group received only saline solution, the second group were treated with reserpine, the third group with estradiole, and the forth group with both reserpine and estradiole. The animals were sacrificed on the 38th day after delivery. There was a statistically significant increase in the weight of the uterus and the ovaries after treatment with estradiole alone, and the same was observed for the group treated with reserpine and estradiole. The latter showed less increase in the uterine weight, which might be due to an impairment of estradiole synthesis caused by reserpine. The wight of the adrenal glands of the immature female rats was increased after treatment with estradiole and reserpine. This implies an involvement of the adrenergic system in the interaction between estradiole and testosterone in immature rats.

Adrenal Glands↗
PubMed1994

Uterotrophic actions of estradiol and tamoxifen are associated with inhibition of uterine insulin-like growth factor binding protein 3 gene expression.

We have recently shown that uterine insulin-like growth factor I (IGF-I) gene expression is up-regulated by tamoxifen, a uterotrophic partial antagonist to the estrogen receptor, but down-regulated by the complete estrogen receptor antagonist ICI 182780, which causes uterine involution. This result is consistent with prior reports indicating that the uterotrophic effects of estradiol are mediated at least in part by estradiol-stimulated uterine IGF-I gene expression. We demonstrate here that the uterotrophic agents estradiol and tamoxifen each suppress expression of the IGF binding protein 3 (IGFBP-3) gene in uterus to less than one-third of control values, while oophorectomy or administration of the complete estrogen receptor antagonist ICI 182780, both of which result in uterine involution, are associated with a greater than 3-fold stimulation of uterine IGFBP-3 gene expression. The data reveal a negative correlation between uterine weight and uterine IGFBP-3 gene expression as well as reciprocal regulation by estradiol of expression in uterus of the genes encoding IGF-I and IGFBP-3. In vitro, IGFBP-3 protein accumulation in media conditioned by primary uterine cultures was decreased by estradiol treatment and increased by ICI 182780 treatment. Together, these observations provide a novel mechanism by which estradiol and antiestrogens modulate uterine IGF-I physiology that is consistent with the view that the mitogenic activity of IGF-I is reduced in the presence of IGFBP-3. The uterotrophic toxicity of chronic estradiol or tamoxifen treatment may be causally related to both the inhibition of uterine IGFBP-3 expression and the stimulation of uterine IGF-I expression by these compounds.

Animals↗