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PubMed1997

Effects of bromocriptine on serum prolactin levels, pituitary weight and immunoreactive prolactin cells in estradiol-treated ovariectomized rats: an experimental model of estrogen-dependent hyperprolactinemia.

The present study was designed to assess the effects of bromocriptine, a dopamine agonist, on pituitary wet weight, number of immunoreactive prolactin cells and serum prolactin concentrations in estradiol-treated rats. Ovariectomized Wistar rats were injected subcutaneously with sunflower oil vehicle or estradiol valerate (50 or 300 micrograms/rat(-1) week (-1) for 2, 4, or 10 weeks. Bromocriptine (0.2 or 0.6 mg rat (-1) day (-1)) was injected daily during the last 5 or 12 days of estrogen treatment. Data were compared with those obtained for intact control rats. Administration of both doses of estrogen increased serum prolactin levels. No difference in the number of prolactin cells in rats treated with 50 micrograms estradiol valerate was observed compared to intact adult animals. In contrast, rats treated with 300 micrograms estradiol valerate showed a significant increase in the number of prolactin cells (P < 0.05). Therefore, the increase inn serum prolactin levels observed in rats treated with 50 micrograms estradiol valerate, in the absence of morphological changes in the pituitary cells, suggests a "functional" estrogen-induced hyperprolactinemia. Bromocriptine decreased prolactin levels in all estrogen-treated rats. The administration of this drug to rats previously treated with 300 micrograms estradiol valerate also resulted in a significant decrease in pituitary weight and number of prolactin cells when compared to the group treated with estradiol alone. The general antiprolactinemic and antiproliferative pituitary effects of bromocriptine treatment reported here validate the experimental model of estrogen-induced hyperprolactinemic rats.

Animals↗
PubMed2004

Biological activity and binding of estradiol to SK-Mel 23 human melanoma cells.

Patients expressing estradiol receptors in melanoma cells have been reported to have a better prognosis. We therefore decided to investigate the in vitro effects of beta-estradiol and tamoxifen on the growth and tyrosinase activity of SK-Mel 23 human melanoma cells. Twenty-four-hour treatment with 0.4 nM beta-estradiol inhibited cell proliferation in 30% (0.70 +/- 0.03 x 10(5) cells) and increased tyrosinase activity in 50% (7130.5 +/- 376.5 cpm/10(5) cells), as compared to untreated cells (1.0 +/- 0.05 x 10(5) cells and 4769 +/- 25.5 cpm/10(5) cells, respectively). Both responses were completely (100%) blocked by 1 microM tamoxifen. Higher concentrations (up to 1.6 nM) or longer treatments (up to 72 h) did not result in a larger effect of the hormone on proliferation or tyrosinase activity. Competition binding assays demonstrated the presence of binding sites to [2,4,6,7-3H]-beta-estradiol, and that the tritiated analogue was displaced by the unlabeled hormone (1 nM to 100 microM, Kd = 0.14 microM, maximal displacement of 93%) or by 10 microM tamoxifen (displacement of 60%). Beta-estradiol also increased the phosphorylated state of two proteins of 16 and 46 kDa, after 4-h treatment, as determined by Western blot. The absorbance of each band was 1.9- and 4-fold the controls, respectively, as determined with Image-Pro Plus software. Shorter incubation periods with beta-estradiol did not enhance phosphorylation; after 6-h treatment with the hormone, the two proteins returned to the control phosphorylation levels. The growth inhibition promoted by estradiol may explain the better prognosis of melanoma-bearing women as compared to men, and open new perspectives for drug therapy.

Antineoplastic Agents, Hormonal↗
PubMed2005

Long-term estradiol deprivation in breast cancer cells up-regulates growth factor signaling and enhances estrogen sensitivity.

Deprivation of estrogen causes breast tumors in women to adapt and develop enhanced sensitivity to this steroid. Accordingly, women relapsing after treatment with oophorectomy, which substantially lowers estradiol for a prolonged period, respond secondarily to aromatase inhibitors with tumor regression. We have utilized in vitro and in vivo model systems to examine the biologic processes whereby long-term estradiol deprivation (LTED) causes cells to adapt and develop hypersensitivity to estradiol. Several mechanisms are associated with this response, including up-regulation of estrogen receptor-alpha (ERalpha) and the MAP kinase, phosphoinositol 3 kinase (PI3-K) and mammalian target of rapamycin (mTOR) growth factor pathways. ERalpha is four- to tenfold up-regulated and co-opts a classical growth factor pathway using Shc, Grb-2 and Sos. This induces rapid non-genomic effects which are enhanced in LTED cells. The molecules involved in the non-genomic signaling process have been identified. Estradiol binds to cell membrane-associated ERalpha, which physically associates with the adaptor protein Shc, and induces its phosphorylation. In turn, Shc binds Grb-2 and Sos, which result in the rapid activation of MAP kinase. These non-genomic effects of estradiol produce biologic effects as evidenced by Elk-1 activation and by morphologic changes in cell membranes. Additional effects include activation of the PI3-K and mTOR pathways through estradiol-induced binding of ERalpha to the IGF-I and epidermal growth factor receptors. A major question is how ERalpha locates in the plasma membrane since it does not contain an inherent membrane localization signal. We have provided evidence that the IGF-I receptor serves as an anchor for ERalpha in the plasma membrane. Estradiol causes phosphorylation of the adaptor protein, Shc and the IGF-I receptor itself. Shc, after binding to ERalpha, serves as the 'bus' which carries ERalpha to Shc-binding sites on the activated IGF-I receptors. Use of small inhibitor (si) RNA methodology to knockdown Shc allows the conclusion that Shc is needed for ERalpha to localize in the plasma membrane. In order to abrogate growth factor-induced hypersensitivity, we have utilized a drug, farnesylthiosalicylic acid, which blocks the binding of GTP-Ras to its membrane acceptor protein, galectin 1, and reduces the activation of MAP kinase. We have also shown that this drug is a potent inhibitor of mTOR as an additional mechanism of inhibition of cell proliferation. The concept of 'adaptive hypersensitivity' and the mechanisms responsible for this phenomenon have important clinical implications. The efficacy of aromatase inhibitors in patients relapsing on tamoxifen could be explained by this mechanism and inhibitors of growth factor pathways should reverse the hypersensitivity phenomenon and result in prolongation of the efficacy of hormonal therapy for breast cancer.

Adaptor Proteins, Signal Transducing↗
PubMed1997

Estradiol and dydrogesterone. A review of their combined use as hormone replacement therapy in postmenopausal women.

The focus of this review is hormone replacement therapy (HRT) with continuous oral 17 beta-estradiol (herein referred to as estradiol) 2 mg/day plus sequential oral dydrogesterone 10 or 20 mg/day for 14 days of each 28-day cycle. According to data from nonblind trials, this regimen relieves climacteric symptoms, preserves bone mineral density (BMD) and improves the cardiovascular risk profile in postmenopausal women. Increases in mean BMD in the lumbar spine of 2.4 to 6.4% have been reported after 2 years' treatment. The effect on BMD of oral estradiol plus sequential dydrogesterone was similar to that achieved with transdermal estradiol plus sequential oral dydrogesterone or with oral tibolone. Good protection against endometrial hyperplasia and cancer is provided by the dydrogesterone component. Cyclical vaginal bleeding occurs in most treatment cycles, but is generally light to moderate and the time of onset is highly predictable. Noncyclical bleeding occurs in < 10% of cycles. Mean serum high density lipoprotein-cholesterol levels are increased and low density lipoprotein-cholesterol levels are decreased during treatment with oral estradiol plus sequential dydrogesterone. Insulin resistance appears to be improved. Blood pressure and bodyweight are not generally affected to any clinically important extent. Serum homocysteine levels were reported to decrease in postmenopausal women with high pretreatment levels. No data are available on the general tolerability profile of this regimen. However, the adverse events that most commonly led to discontinuation of treatment in clinical trials were typical of those associated with HRT, including vaginal bleeding headache, bloating and breast tenderness. Although the risk of breast cancer has not been specifically assessed for this regimen, it is unlikely to carry a greater risk than that of other HRT regimens. In summary available data indicate that treatment with continuous oral estradiol plus sequential dydrogesterone is effective in relieving climacteric symptoms and preserving BMD in postmenopausal women. The dydrogesterone component provides good endometrial protection and cycle control without negating the cardiovascular benefits of estradiol. Comparisons with other standard HRT regimens and long term data (including clinical end-points) are needed. In the meantime, this regimen can be regarded as an acceptable HRT option.

Aged↗
PubMed1984

In vitro testosterone secretion by testicular tissue from young bulls and the effects of chronic and acute exposure to estradiol-17 beta.

The possibility that estradiol-17 beta may directly influence testicular steroidogenesis in bulls was investigated in vitro. Testicular tissues were incubated for 4 h and regression coefficients (b, ng X ml-1 X h-1) based on the increase in testosterone in the medium were used to describe testosterone secretion rates. In the first experiment, testicular tissues from control bulls and bulls chronically implanted with estradiol were incubated in the absence (basal conditions) or presence of 10 mIU/ml human chorionic gonadotropin (hCG). Under basal conditions, testosterone secretion rates were similar for tissues from control (b = 24.1 +/- 6.0) and implanted (b = 34.7 +/- 6.0) bulls. Testosterone secretion rates were increased approximately fourfold during incubation with hCG; tissues from implanted animals secreted testosterone at a higher rate (P less than .05) than control tissues (b = 120.7 +/- 6.0 vs 81.6 +/- 6.0). In a second experiment, testicular tissues were obtained from control bulls and incubated both with and without hCG (10 mIU/ml) and with and without estradiol (concentrations ranging from 3.7 nM to 37 microM). In this experiment, basal secretion rate (b = 12.6 +/- 3.6) was increased threefold during incubation with hCG (b = 37.8 +/- 3.6). Estradiol failed to inhibit hCG-stimulated testosterone secretion when bovine testicular tissue was incubated with 0, 3.7 and 370 nM estradiol. In contrast, 37 microM estradiol suppressed (P less than .05) testosterone secretion, perhaps reflecting a pharmacologic effect. The results suggest that neither chronic nor acute exposure to estradiol directly affects testosterone secretion by the bovine testis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Ovulation in postpartum beef cows treated with estradiol.

The effect of implants of estradiol on initiation of ovarian cycles postpartum was studied in 201 anestrous beef cows. Cows from four farms were used over a 2-yr period in a 2 x 3 factorial arrangement of treatments with estradiol implants and stage postpartum as main effects. Cows were assigned at random within date of calving within farm to receive an ear implant containing estradiol-17 beta (24 mg) for 21 d or to serve as controls. Stages postpartum at implantation were divided into less than or equal to 25, 26 to 39, and greater than or equal to 40 d, three stages that should reflect potential changes in hypothalmic-hypophysial sensitivity to estradiol. Blood samples for determination of progesterone were obtained and rectal examinations of the ovaries performed at implant insertion, 14 d after insertion, at implant removal (d 21), and 14 d after removal (d 35) to assess ovulatory response to treatment. Circulating concentrations of estradiol on d 14 of treatment averaged 3.2 +/- 1.0 and 23.1 +/- 4.7 pg/ml for control and estradiol-treated cows, respectively. Compared with control cows, treatment with estradiol initiated after d 26 postpartum increased the proportion of cows that ovulated during the experimental period. No differences were seen in the average days postpartum when cows were first determined to have ovulated.

Anestrus↗
PubMed1997

Twenty-four-hour basal and repetitive pentagastrin-stimulated gastric acid secretion in normal and sham-operated rats and in rats after gonadectomy or treatment with estradiol or testosterone.

BACKGROUND: Studies in different species have suggested, but not established, that sex hormones influence gastric acid secretion. We studied how acid output is affected by the sex hormones estradiol or testosterone in vivo and in vitro. METHODS: In gastric fistula rats that were normal, sham-operated, neonatally gonadectomized, or treated with estradiol or testosterone, 24-h basal and pentagastrin-stimulated acid secretion was measured. The in vitro effects of estradiol and testosterone on histamine-induced aminopyrine accumulation in isolated parietal cells were also determined. RESULTS: Basal acid output was similar in the two sexes, but stimulated secretion was significantly higher (34%; P < 0.01) in males. Ovariectomy did not influence acid output, whereas orchidectomy reduced basal (18%; NS) and stimulated 24-h secretion (P < 0.01). Estradiol decreased (23%; NS) the 24-h basal output in females but not in males. Estradiol suppressed stimulated secretion in females (29%, P < 0.01) and males (42%, P < 0.01) during the day. At night the stimulated secretion increased in both females (17%, NS) and males (32%, P < 0.05). A similar pattern was found when rats were treated with testosterone. In vitro, estradiol and testosterone reduced histamine-stimulated aminopyrine accumulation in both female and male isolated parietal cells. CONCLUSIONS: Estradiol and testosterone both appear to influence gastric secretion in rats, and their action differs between day and night, between the sexes, and between basal and stimulated secretion.

Aminopyrine↗
PubMed1975

Transitory changes in plasma progestins, estradiol, and luteinizing hormone approaching ovulation in the bovine.

Progestins, estradiol, and luteinizing hormone were measured by radioimmunoassay in bovine plasma samples collected from indwelling jugular catheters daily on days minus 6 to minus 4, every 6 h on days minus 3 and minus 2, and every 2 h from day minus 1 to ovulation. Least squares analyses characterized time trends within animals and interrelationships between these hormones. Plasma progestins decreased from 5.7 ng/ml at day minus 6 to .07 ng at the peak of luteinizing hormone. No preovulatory peripheral increase in plasma progestins was detected. Estradiol increased from 2 pg/ml at day minus 4 to 6 pg at minus 12 h and then increased abruptly to 7.4 pg at the peak of luteinizing hormone. This matter increase in estradiol was synchronous with the acute preovulatory surge of luteinizing hormone. Association was positive between estradiol and luteinizing hormone, but negative between progestins and estradiol. Estradiol decreased 50% by 5 h following the peak of luteinizing hormone with a return to base (2 pg) at 14 h. An increase of .1 ng luteinizing hormone/ml plasma per day was linear from day minus 6 to 8 h prior to the luteinizing hormone peak. Luteinizing hormone increased to a peak of 13.5 ng/ml and remained elevated for 10.5 h. These results are consistent with the hypothesis that an increase at proestrus in estradiol rather than progestins triggers the preovulatory surge of luteinizing hormone in the bovine.

Animals↗
PubMed1982

Lipotropic effect of estradiol-17 beta in fed and fasted lactating cows.

The lipotropic effect of estradiol-17 beta was measured in seven nonpregnant Holstein-Friesian cows 2 to 5 wk into lactation. The experiment was divided into an initial 3-day control period, 19 days treatment, and 2 days fast. Jugular blood samples were taken twice daily during the control period, the last 2 days of treatment, and the fast. After the control period, four cows received daily injections of estradiol-17 beta benzoate (15 mg) in sesame oil for the remainder of the experiment whereas three cows received injections of sesame oil only. Estradiol-17 beta did not change triglyceride concentration of plasma during the treatment period but increased it markedly during fast. Estradiol-17 beta increased the free glycerol concentration of plasma during treatment. Cholesterol concentrations of plasma showed a consistent trend lower in the estradiol group during treatment and fast. No differences were apparent in glucose and blood ketone concentrations. The concentration of insulin in plasma was lower for the estradiol group during treatment. Estradiol-17 beta appears to have a similar effect on lipid metabolism in dairy cows to other species. However, it exerted a strong lipotropic effect only under fasting.

3-Hydroxybutyric Acid↗
PubMed1987

Influence of stage of cycle, corpus luteum location, follicle size, and number of large follicles on estradiol-17 beta concentrations in bovine follicles.

Concentrations of estradiol-17 beta in follicular fluid were correlated to follicular size, stage of estrous cycle, location of corpus luteum, and presence of large follicles. Paired ovaries were obtained from 481 nonpregnant cows at slaughter and follicles were classified as ipsilateral or contralateral to the corpus luteum. Follicular fluid estradiol-17 beta concentrations from 2494 small, 1485 medium, and 396 large follicles were quantified by radioimmunoassay. Stage of estrous cycle was estimated by visual examination of the corpus luteum. Follicles in stage 1 of the estrous cycle (d 1 to 4) had the highest estradiol-17 beta concentration and the smallest mean follicular diameter. Location of follicles relative to the corpus luteum had no influence on estradiol-17 beta concentrations. As follicular size increased, concentration of estradiol-17 beta also increased. The presence of a single large follicle did not affect the concentration of estradiol-17 beta in medium or small follicles. In contrast, if multiple large follicles occurred in the same cow, concentrations of estradiol-17 beta were significantly lower in medium but not small follicles.

Animals↗
PubMed1978

Plasma concentration of progesterone and estradiol during the ovulatory cycle of the turkey.

Radioimmunoassays were used to estimate concentrations of progesterone and estradiol in the peripheral plasma of hens in relation to the first (C1) or second (C2) ovulation in a sequence. Peak concentrations of progesterone were found at 6--3 hr. before ovulation. There were no consistent changes in estradiol concentrations. When blood samples were taken at 2-hr. intervals for 24--48 hrs., estradiol concentrations peaked at 18 hours before C1 ovulation and during the same time of day (2--6 p.m.) during the period of no ovulation between sequences, but no estradiol peak preceded C2 ovulation. When blood samples were taken from a second population of hens at 1-hr. intervals during the 12 hr. period before expected C2 ovulation, a significant rise in estradiol (P less than 0.01) was associated with the preovulatory peak of progesterone. The preovulatory peak of estradiol in these hens may be linked to a seasonally high rate of secretion of both estradiol and progesterone. As estimated indirectly by hypophysectomy, release of an ovulatory amount of LH in the turkey coincided with the rise of progesterone to the preovulatory peak.

Animals↗
PubMed1996

Influence of 17- alpha-estradiol on catecholamine secretion from the perfused rat adrenal gland.

OBJECTIVES: It has been known that adrenal corticosteroids influence the expression of adrenomedullary catecholamine-synthetizing enzymes and also suppress the emission of axonal-like processes in cultured chromaffin cells. In the present study, it was attempted to investigate the effect of 17-alpha-estradiol on catecholamine (CA) secretion evoked by acetylcholine (ACh). DMPP. McN-A-343, excess K+ and Bay-K-8644 from the isolated perfused rat adrenal gland. METHODS: Mature male Sprague-Dawley rats were anesthetized with ether. The adrenal gland was isolated by the method of WaKade. A cannula used for perfusion of the adrenal gland was inserted into the distal end of the renal vein. The adrenal gland, along with ligated blood vessels and the cannula, was carefully removed from the animal and placed on a platform of a leucite chamber. RESULTS: The perfusion of 17-alpha-estradiol (1-100 uM) into an adrenal vein for 20 min produced relatively dose-dependent inhibition in CA secretion evoked by ACh (5.32 mM). DMPP (100 uM for 2 min). McN-A-343 (100 uM for 2 min) and Bay-K-8644 (10 uM for 4 min), while it did not affect the CA secretory effect of high K+ (56 mM). Also, in the presence of 17-beta-estradiol. CA secretion of ACh. DMPP and McN-A-343, without any effect on excess K(+)-evoked CA sectretion was depressed. However, in adrenal glands pre-loaded with 17-alpha-estradiol (10 uM) plus tamoxifen (2 uM), which is known to be a selective antagonist of estrogen receptors (for 20 min). CA secretory responses evoked by ACh. DMPP and McN-A-343 were condiderably recovered as compared to that of 17-alpha-estradiol only, but excess K(+)-induced CA secretion was not affected. However, pre-treatment with 17-alpha-estradiol in the presence of meclopramide (dopaminergic antagonist) did not affect the secretory effect of CA evoked by ACh. DMPP, McN-A-343 and high potassium. CONCLUSIONS: These results suggest that 17-alpha-estradiol causes the marked inhibition of CA secretion evoked by cholinergic receptor stimulation, but not that by excess K+, indicating strongly that this effect may be mediated by inhibiting the influx of extracellular calcium into the rat adrenomedullary chromaffin cells through the activation of inhibitory estrogen receptors, and it also plays a modulatory role in regulating CA secretion.

Adrenal Glands↗
PubMed2001

Changes in testosterone, cortisol, and estradiol levels in men becoming fathers.

OBJECTIVE: To quantify longitudinally steroid hormone (testosterone, cortisol, and estradiol) concentrations in men becoming fathers for the first time ("dads"). SUBJECTS AND METHODS: Volunteer study subjects were recruited from first-trimester prenatal classes in Kingston, Ontario, in February 1999. Twenty-three dads provided saliva samples from recruitment through 3 months after the birth of their children. Fourteen men who were not fathers were recruited from the general population to serve as age-matched controls for season and time of day. Estradiol, testosterone, and cortisol levels were quantified. RESULTS: After controlling for effects of time of day and season, dads had lower mean +/- SE testosterone (6.5+/-0.7 vs 10.0+/-0.9 ng/dL; P<.005) and cortisol (morning values, 0.30+/-0.05 vs 0.53+/-0.05 microg/dL; P<.005) concentrations, a higher proportion of samples with detectable estradiol concentrations (68% [308/454] vs 57% [87/154]; P=.01), and higher estradiol concentrations in those detectable samples (3.81+/-0.09 pg/mL [13 dads] vs 3.26+/-0.11 pg/mL [9 controls]; P<.002) than did control men. Within 10 individual dads with frequent samples before and after the birth, the percentage of samples with detectable estradiol was lower during the month before the birth than during the month after (51% vs 71%; P=.02), and cortisol concentration was increased in the week before the birth (to a mean of 0.16 microg/dL). In each of 13 dads providing frequent samples, testosterone concentration and variance were low immediately after the birth (no change from previous levels in 5, decrease after prebirth increase in 3, and decrease relative to all other times in 5). CONCLUSIONS: In this population of Canadian volunteers attending prenatal classes, expectant fathers had lower testosterone and cortisol levels and a higher proportion of samples with detectable estradiol concentrations than control subjects. Individual patterns of testosterone variance relative to the birth and estradiol and cortisol concentrations immediately before the birth may be worthy of further investigation. The physiologic importance of these hormonal changes, if any, is not known. However, they are hormones known to influence maternal behavior.

Adult↗
PubMed2006

Pharmacokinetic interaction between bosentan and the oral contraceptives norethisterone and ethinyl estradiol.

OBJECTIVE: Bosentan has been shown in vitro and in vivo to induce the cytochrome P450 enzymes CYP2C9 and CYP3A4. The present study was conducted to investigate the effect of bosentan on the pharmacokinetics of a combined oral contraceptive. SUBJECTS AND METHODS: In a randomized, 2-way crossover study, 20 healthy female subjects received Treatments A and B. Treatment A consisted of a single dose of OrthoNovum containing 1 mg norethisterone (norethindrone) and 35 microg ethinyl estradiol. Treatment B consisted of bosentan, 125 mg b.i.d. for 7 days plus concomitant norethisterone and ethinyl estradiol on Day 7. Plasma concentrations of norethisterone and ethinyl estradiol were measured on days of oral contraceptive administration. RESULTS: In the absence of bosentan, the pharmacokinetics of norethisterone and ethinyl estradiol were characterized by Cmax and AUC0-infinity values (95% CI) of 9.8 (8.1, 11.9) ng/ml and 72.9 (57.0, 93.1) ng x h/ml, and 53.0 (47.0, 59.9) pg/ml and 758 (655, 878) pg x h/ml, respectively. Concomitant bosentan did not affect the Cmax but significantly decreased the AUC of norethisterone and ethinyl estradiol by 13.7% (-23.5, -2.6) and 31.0% (-40.5,-20.2), respectively. The maximum decrease in AUC of norethisterone and ethinyl estradiol in an individual subject was 56% and 66%, respectively. CONCLUSIONS: Bosentan decreases the AUC of norethisterone and ethinyl estradiol in healthy female subjects. In patients treated with bosentan, reduced efficacy of hormonal contraceptives should be considered.

Adult↗
PubMed1997

Can luteal phase serum estradiol concentrations predict karyotypes of spontaneous abortions?

Low serum estradiol concentrations during pregnancy have been associated with spontaneous abortions. A large proportion of abortuses have chromosomal abnormalities. To determine whether serum estradiol during the luteal phase of conception cycles can predict the karyotype of spontaneous abortions, serum estradiol samples were drawn 11 days after embryo transfer from 52 women who subsequently had spontaneous abortions and chromosomal analysis was performed on the products of conception. The frequency of estradiol levels < 100 pg/ml was compared between normal and abnormal karyotypic spontaneous abortions. Chromosomal analyses among 52 spontaneous abortions revealed 14 (27%) to be normal and 38 (73%) abnormal. Among the 38 karyotypic abnormalities 30 were aneuploidy and eight were polyploidy. Serum estradiol levels were < 100 pg/ml in eight women (15%) and > 100 pg/ml in 44 women (85%). The frequencies of estradiol < 100 pg/ml in spontaneous abortions with normal (7%) and abnormal (18%) karyotypes were not significantly different. Thus, serum estradiol cannot predict the karyotype of spontaneous abortions.

Abortion, Spontaneous↗
PubMed1999

Augmentation and suppression of action potentials by estradiol in the myometrium of pregnant rat.

The purpose of this study was to investigate the actions of estradiol on spontaneous and evoked action potentials in the isolated longitudinal smooth muscle cells of the pregnant rat. Single cells were obtained by enzymatic digestion from pregnant rat longitudinal myometrium. Action potentials and currents were recorded by whole-cell current-clamp and voltage-clamp methods, respectively. The acute effects of 17beta-estradiol on action potentials and inward and outward currents were investigated. The following results were obtained. The average resting membrane potential of single myometrial cells was -54 mV (n = 40). In many cells, an electrical stimulation evoked a membrane depolarization, and action potentials were superimposed on the depolarization. In some cells, spontaneous action potentials were observed. Estradiol (30 microM) slightly depolarized the membrane (ca. 5 mV) and attenuated the generation of action potentials by reducing the frequency and amplitude of the spikes. Afterhyperpolarization was also attenuated by estradiol (30 microM). On the other hand, in 5 of 35 cells, estradiol increased the first spike amplitude and action potential duration, while frequency of the spike generation and afterhyperpolarization were inhibited. In voltage-clamped muscle cells, estradiol inhibited both inward and outward currents. Acute inhibition or augmentation of spike generation by estradiol is due to the balance of inhibition of inward and outward currents. Inhibition of both currents also prevented afterhyperpolarization, causing potential-dependent block of Ca spikes.

Action Potentials↗
PubMed1999

The normal breast epithelium of women with breast cancer displays an aberrant response to estradiol.

Breast epithelial response to estradiol may play an important role in breast cancer etiology. We have examined the relationship between serum estradiol and progesterone levels and normal breast epithelial expression of estrogen receptor (ER) alpha, progesterone receptor (PgR), and epithelial proliferation (as reflected by the Ki-67 labeling index) in 121 women (50 newly diagnosed breast cancer cases and 71 benign breast disease controls). Simultaneous samples of grossly normal breast tissue and venous blood were obtained from women undergoing breast surgery. Serum estradiol and progesterone levels were measured by radioimmunoassay; breast epithelial ER, PgR, and Ki-67 expression was measured by immunohistochemistry. Linear regression, controlled for patient age and ductal and lobular composition of the tissue, showed that the breast epithelium of control women displayed an inverse correlation between serum estradiol and ER-alpha, which was not seen in case women (P for the difference in regression slopes = 0.001). PgR expression displayed a significant positive correlation with serum estradiol in cases, but not in controls. Epithelial proliferation had no relationship to either estradiol or progesterone in both cases and controls but showed an inverse relationship with ER in controls and a direct relationship in cases (P for the difference in regression slopes = 0.066). These results suggest a dysregulation of hormonal response in the normal breast epithelium of high-risk women, with lack of regulation of ER by estradiol, increased estrogen responsiveness as reflected by PgR expression, and a dissociation of ER expression and proliferative response.

Adult↗
PubMed1979

[Characteristics of protein-protease inhibitors, 17-beta estradiol and progesterone in the blood of heifers returning to estrus following LH/FSH-RH treatment].

Tests were performed to study the inhibitive capacity of protein-protease inhibitors, 17-beta estradiol, and progesterone in the blood serum of 21 heifers returning to oestrus which had been treated intramuscularly with 400 microgram LH/FSH-RH. Four selected heifers were examined as to the relationships between the concentrations of 17-beta estradiol, progesterone and the inhibitive capacity of the serum. Heifer no. 1 had low concentrations of 17-beta estradiol and higher concentrations of progesterone (average levels 7.8 and 657.4 pg ml-1 of serum). On the other hand, heifer no. 4 was found to have higher concentration of 17-beta estradiol and lower values of progesterone (average levels 28.3 and 325 pg ml-1 of serum). Having shown heat, the heifers were fertilized and remained in calf. Heifer no. 2 with a low concentration of progesterone (292 pg ml-1 of serum) and 17-beta estradiol (12.4 pg ml-1 of serum), as well as heifer no. 3 with a high concentration of both (830 pg ml-1 of serum and 22.7 pg ml-1 of serum, respectively) showed no heat and they were not mated. Heifers with significant differences in the concentrations of progesterone and 17-beta estradiol and with low values of protein-protease inhibitory capacities remained in-calf, whereas heifers with lower progesterone and 17-beta estradiol values, or adversely, with higher inhibition values, showed no heat. Synthetic LH/FSH-RH was found not to increase the amount of protein-protease inhibitors in heifer serum, as distinct from the cervical mucus of breeding cows treated with gestagens in heat synchronization.

Animals↗