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At least 451 records · Page 25Linked to original sources
PubMed1986

Estrogenic activities of estradiol enantate and ethinylestradiol compared at a clinical level.

Healthy menopausic women accepted to receive two consecutive estrogenic treatments: 1. ethinylestradiol 0.030 mg/d p.o. during 21 days; 2. a single dose of estradiol enantate (estra-1,3,5(10)-triene-3-ol-17 beta-heptanoate, one of the components of Perlutal or Topasel) 10 mg i.m. Both treatments were separated by a 1-month wash-out period, without any medicine. FSH, LH and prolactin serum levels were measured in each one of the subjects by radioimmunoassay before the beginning of each treatment and for at least 14 times during 31 days thereafter. A temporary decrease of the FSH levels and a temporary increase of the prolactin levels were induced by both treatments. In this respect the estradiol enantate effect was more precocious but the quality and the magnitude of the responses were similar among the two substances. The LH profile evolution was different: there was a decrease under estradiol enantate, but a very sharp increasing peak was observed on the 17th day under ethinylestradiol. By comparing the obtained results no significant statistical differences between the estrogenic potencies of the therapeutic schemes applied were found.

Clinical Trials as Topic↗
PubMed1980

Combined use of clomiphene and intranasal luteinizing hormone-releasing hormone for induction of ovulation in chronically anovulatory women.

Combined therapy with clomiphene and intranasal luteinizing hormone-releasing hormone (LHRH) was used to induce ovulation in eight chronically anovulatory patients under treatment for infertility. Clomiphene, 100 mg daily, was given from the 5th to the 9th day of the cycle. Synthetic LHRH was administered intranasally in different dosages from day 11 to day 14, in an attempt to induce late follicular development and ovulation. Five of the eight patients ovulated, and three conceived. The success achieved with combined clomiphene and intranasal LHRH administration suggests a therapeutic potential in the management of anovulatory infertility.

Administration, Intranasal↗
PubMed1985

[Degree of manifestation of therapeutic pathomorphosis and the nature of the change in the estrogen and progesterone receptors after the radiation and chemotherapy of breast cancer].

Estradiol and progesterone receptor levels were measured in 130 patients with stage III breast tumors before treatment and following preoperative radiation or chemotherapy. The data were evaluated versus the morphologic features of posttreatment pathomorphosis of tumor. Standard fractionated radiation (total dose of 70 Gy) was followed by pronounced postradiation pathomorphosis and a decrease in the level and incidence of steroid receptors in 72.7-87.5%. The essentially unchanged receptor profile of tumor following large-fraction (total dose-20 Gy) irradiation as well as presence of estradiol and progesterone receptors in the originally receptor-negative neoplasms after chemotherapy were matched by a slight degree of pathomorphosis.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2001

Requirement of Ras-dependent pathways for activation of the transforming growth factor beta3 promoter by estradiol.

It has been previously observed that the transforming growth factor beta3 (TGFbeta3) gene can be activated by both estradiol (E(2)) and selective estrogen receptor modulators (SERMs) in vivo but that only SERMs have a potent stimulatory effect on the TGFbeta3 promoter in cultured cells. We demonstrate in this report that E(2) can act also as a potent inducer of the TGFbeta3 promoter via a novel and specific estrogen receptor (ER)alpha-mediated mechanism. Our results show that treatment with epidermal growth factor or transfection of a constitutively active Ras mutant allows E(2) to induce the TGFbeta3 promoter via ERalpha in cotransfected HeLa and osteosarcoma MG63 cells. Both protein kinase C (PKC) and mitogen-activated protein kinase (MAPK) inhibitors can block the combined stimulatory effect of E(2) and epidermal growth factor/Ras. However, E(2) induction of the TGFbeta3 promoter was found to be unaffected by mutation of ERalpha serine 118, a well-characterized target of MAPK. Progressive deletion analysis of the ERalpha amino-terminal region delineated three separate domains modulating the E(2)/activated Ras response, revealing a complex functional organization of the ERalpha A/B domain required for regulation of the TGFbeta3 promoter. In addition, PKC and MAPK inhibitors had no effect on the induction of TGFbeta3 promoter activity by the SERM EM-652. These results indicate that induction of the TGFbeta3 promoter by the E(2)/ERalpha complex requires the concomitant activation of PKC and MAPK signaling and provide a novel framework for the design of more effective estrogen-based therapeutic strategies.

Enzyme Inhibitors↗
PubMed1992

Recent data on estrogen sulfatases and sulfotransferases activities in human breast cancer.

Of the total number of breast cancers approx. 30-50% are hormone-dependent and estradiol is one of the main factors of cancerization. Consequently, the control of this hormone inside the cancer cell is of capital importance because it is well established that the inhibition of estradiol biosynthesis can have a positive effect on the evolution of the disease. The blockage of estradiol can be obtained by the action of anti-aromatases, anti-sulfatases, the control of the 17 beta-hydroxysteroid dehydrogenase activity or by the stimulation of the sulfotransferase which converted the estrogens in their sulfates. In breast cancer tissue estrone sulfate is quantitatively the most important source of estradiol. In the intact cell, estrone sulfatase activity is very intense in the hormone-dependent cell lines (e.g. MCF-7, T-47D) but very small activity is observed in the hormone-independent (e.g. MDA-MB-231, MDA-MB-436) cell lines. However, this activity became very strong after homogenization in the hormone-independent cells, suggesting the presence of repressive factor(s) for this enzyme or its sequestering in an inactive form, in the intact cells of these cell lines. In a series of previous studies it was found that in hormone-dependent cell lines different anti-estrogens: tamoxifen and derivatives, ICI 164,384, very significantly decrease the estradiol concentration originated from estrone sulfate, and recently it was observed that Decapeptyl (D-Trp6-gonadotropin-releasing hormone) in the presence of heparin can also decrease the conversion of estrone sulfate into estradiol. No significant effect was obtained in the presence of heparin or Decapeptyl alone. The estrone sulfatase activity can be inhibited by progesterone, the progestagen R-5020, and testosterone. In another series of recent studies the presence of very strong estrogen sulfotransferase activity has been shown in one breast cancer cell line, the MDA-MB-468. We can conclude that: (1) the control of estradiol concentration can be carried out in the breast cancer tissue itself; (2) estrone sulfate can play an important role in the bioavailability of estradiol in the breast cancer cell; and (3) as is the case for the aromatase, the control of: the estrogen sulfatase, estrogen sulfotransferase, and 17 beta-hydroxysteroid dehydrogenase can be new targets for therapeutic applications in breast cancer.

Breast Neoplasms↗
PubMed1999

17beta-estradiol reduces stroke injury in estrogen-deficient female animals.

BACKGROUND AND PURPOSE: The importance of postmenopausal estrogen replacement therapy for stroke in females remains controversial. We previously showed that female rats sustain less infarction in reversible middle cerebral artery occlusion (MCAO) than their ovariectomized counterparts and that vascular mechanisms are partly responsible for improved tissue outcomes. Furthermore, exogenous estrogen strongly protects the male brain, even when administered in a single injection before MCAO injection. The present study examined the hypothesis that replacement of 17beta-estradiol to physiological levels improves stroke outcome in ovariectomized, estrogen-deficient female rats, acting through blood flow-mediated mechanisms. METHODS: Age-matched, adult female Wistar rats were ovariectomized and treated with 0, 25, or 100 microgram of 17beta-estradiol administered through a subcutaneous implant or with a single Premarin (USP) injection (1 mg/kg) given immediately before ischemia was induced (n=10 per group). Each animal subsequently underwent 2 hours of MCAO by the intraluminal filament technique, followed by 22 hours of reperfusion. Ipsilateral parietal cortex perfusion was monitored by laser-Doppler flowmetry throughout ischemia. Cortical and caudate-putamen infarction volumes were determined by 2,3, 5-triphenyltetrazolium chloride staining and digital image analysis. End-ischemic regional cerebral blood flow was measured in ovariectomized females with 0- or 25-microgram implants (n=4 per group) by (14)C-iodoantipyrine quantitative autoradiography. RESULTS: Plasma estradiol levels were 3.0+/-0.6, 20+/-8, and 46+/-10 pg/mL in the 0-, 25-, and 100-microgram groups, respectively. Caudate-putamen infarction (% of ipsilateral caudate-putamen) was reduced by long-term, 25-microgram estrogen treatment (13+/-4% versus 31+/-6% in the 0-microgram group, P<0.05, and 22+/-3% in the 100-microgram group). Similarly, cortical infarction (% of ipsilateral cortex) was reduced only in the 25-microgram group (3+/-2% versus 12+/-3% in the 0-microgram group, P<0.05, and 6+/-3% in the 100-microgram group. End-ischemic striatal or cortical blood flow was not altered by estrogen treatment at the neuroprotective dose. Infarction volume was unchanged by acute treatment before MCAO when estrogen-treated animals were compared with saline vehicle-treated animals. CONCLUSIONS: Long-term estradiol replacement within a low physiological range ameliorates ischemic brain injury in previously ovariectomized female rats. The neuroprotective mechanism is flow-independent, not through preservation of residual ischemic regional cerebral blood flow. Furthermore, the therapeutic range is narrow, because the benefit of estrogen in transient vascular occlusion is diminished at larger doses, which yield high, but still physiologically relevant, plasma 17beta-estradiol levels. Lastly, unlike in the male brain, single-injection estrogen exposure does not salvage ischemic tissue in the female brain. Therefore, although exogenous steroid therapy protects both male and female estrogen-deficient brain, the mechanism may not be identical and depends on long-term hormone augmentation in the female.

Animals↗
PubMedDate not supplied

[Therapeutic results with tamoxifen in oligospermia. II. Hormonal analysis and semen parameters].

During a five months lasting treatment with tamoxifen (2 X 10 resp. 2 X 20 mg daily) a significant increase of testosterone, LH, FSH, estradiol, free testosterone and SHBG was found. The prolactin levels diminished. In semen analysis the values of pH and fructose decreased within the normal range. The sperm density increased significantly, but we could not ascertain whether a dosage of 2 X 20 mg/die will provide better therapeutic results. Furthermore the hormonal and seminal investigations described in this paper did not allow to predict those patients who would be good responders on tamoxifen therapy. Tamoxifen seems to be effective in normo-, but also in hypo- and hypergonadotropic patients.

Estradiol↗
PubMed2003

A comparison of the anti-inflammatory activities of conjugated estrogens and 17-beta estradiol.

OBJECTIVE AND DESIGN: Unregulated chronic inflammatory process partly due to an estrogen deficiency may render postmenopausal women vulnerable to degenerative conditions such as arthritis, osteoporosis, atherosclerosis, and Alzheimer's disease. Current confusion regarding therapeutic efficacy of estrogen replacement therapy may be due to different estrogen formulations used, short term therapy, as well as advanced stage of the disease. MATERIALS AND METHODS: We compared anti-inflammatory activities of two major estrogen preparations, conjugated equine estrogen (CEE) and 17-beta estradiol, using an animal model (rat mesentery) of in vivo inflammatory reaction to intravenously infused amyloid-beta, examined by video recording and subsequently analyzed by transmission electron microscopy. Cellular markers of inflammation were monitored: leukocyte migration, platelet activation, mast cell activation/degranulation, and endothelial disruption. RESULTS: Low doses of CEE (0.3 mg/kg for 3 weeks) demonstrated significant anti-inflammatory activity, whereas even at high doses (2.0 mg) 17-beta estradiol had only minimal activity. CONCLUSION: CEE, a mixture of several compounds, may have some component(s) with significant anti-inflammatory activity. The anti-inflammatory activity of CEE may have a role in prevention of several degenerative diseases associated with menopause.

Amyloid beta-Peptides↗
PubMedDate not supplied

Effect of intracoronary estradiol on postischemic microvascular damage in a porcine model: a myocardial contrast echocardiographic study.

Coronary microvascular damage can occur in the presence of myocardial ischemia even if epicardial vessels are patent, a phenomenon known as "no-reflow." Estrogens have favorable effects on coronary conductance and resistance arteries, and may have therapeutic value in ischemic syndromes. Myocardial contrast echocardiography (MCE) is a promising method for evaluating microvascular damage. In this study, the authors hypothesized that acute intracoronary 17beta-estradiol administration can reduce postischemic microvascular damage, which is evaluated by MCE, in a porcine model. Sixteen male pigs were randomized into 2 groups: the treatment group (n = 9) received intracoronary estradiol in increasing doses, and the control group (n = 7) received intracoronary vehicle (dimethylsulfoxide, DMSO). Microvascular damage was induced by balloon catheter occlusion followed by reperfusion of the left circumflex coronary artery (LCX). MCE using Levovist with harmonic imaging was performed before and during 15-minute balloon occlusion of the proximal LCX to determine perfusion areas of the left anterior descending artery (LAD) and LCX. MCE was performed immediately postocclusion and after each injection of estradiol (1, 10, and 100 nmol/L) or DMSO. Videodensitometry measurements were performed as a quantitative marker for myocardial microvascular damage. Videodensitometry results were expressed as peak intensity ratios. Intracoronary estradiol induced a significant reduction in myocardial microvascular damage after ischemic episode by videodensitometry measurements when compared to intracoronary DMSO. The authors conclude that intracoronary injection of estradiol reduces postischemic microvascular damage measured by MCE in a porcine model.

Animals↗
PubMed1980

[Correlation betwen the 17-beta-estradiol content in the blood and the estrogen excretion level in pergonal-500 stimulation of ovulation].

Correlation between 17 beta-estradiol blood content and the excretion of estrogens was studied during 19 cycles in 10 women with amenorrhea treated with pergonal-500. A high degree of correlation between two lines of values has been observed (r = 0.89 +/- 0.03). It is concluded that both methods are equally informative in the evaluation of pergonal therapeutic effect.

Adult↗
PubMed1989

Development and application of a radioimmunoassay of the new progestagen gestodene.

A radioimmunoassay for the determination of gestodene (17-ethinyl-13-ethyl-17 beta-hydroxy-4,15-gonadien-3-one) in human plasma is described with regard to procedure, specificity, accuracy and reproducibility. Antiserum was raised against gestodene-3-O-(carboxymethyl)oxime-BSA in rabbits and [9,11-3H]-gestodene tracer was used with a specific radioactivity of 2.16 TBq/mmol. The final antiserum dilution was 1: 200,000. RIA was performed according to routine methods using diethylether plasma extracts and the charcoal separation technique. Cross-reactivity of antiserum with cortisol, 17 beta-estradiol, progesterone, testosterone and ethinylestradiol was less than 0.03%; levonorgestrel exhibited a 5% cross-reactivity. No cross-reactivity with metabolites of gestodene or ethinylestradiol was found. Accuracy and precision of the assay were tested using human plasma samples spiked with 1, 5 and 10 ng/ml gestodene. Accuracy was within 94 to 104% of the nominal values. Within-assay and between-assay coefficients of variation were in the range of 4.7-6.5% and 10.3-13.1%, resp. This RIA was used to follow plasma gestodene levels after single oral administration of 75 micrograms of gestodene combined with 30 micrograms ethinylestradiol as tablet and coated tablet in a cross-over design in 6 female test subjects. Plasma gestodene levels were equivalent after both treatments.

Analysis of Variance↗
PubMed2005

Improvement in embryo recovery using double uterine flushing.

The objective of the present study was to evaluate the effects of double uterine flushing on the recovery of embryos/ova in cattle. Two hundred and ten embryo recovery procedures were conducted using a double uterine flushing method, and the results were compared with 432 conventional single-flushing procedures. Cyclic Limousin (n = 403) and Guzera (n = 239) donor cows received an intravaginal progesterone releasing device and 2 mg of estradiol benzoate on Day 0. Between Days 5 and 9, donors received decreasing doses of FSH, which ranged from 200 to 300 IU (Bos indicus) and 300 to 500 IU (Bos taurus). On the afternoon of Day 7, donors received an injection of 500 microg cloprostenol and progesterone implants were removed 12 h later (morning of Day 8). Artificial insemination was performed between 14 and 26 h after first detection of behavioral estrus. Cows were randomly assigned to have embryos recovered by a double-flushing method (n = 210) or the conventional single-flushing procedure (n = 432). For the double-flushing procedure, after first flushing the whole uterus with 1L of Dubelco's Phosphate Buffered Saline (DPBS), a Foley catheter was positioned in the uterine body to permit refilling of the uterus with fresh DPBS (80-150 mL). The catheter was closed with the plunger of a disposable 5 mL syringe, and the donors were allowed to rest in a holding area for 30 min. Thereafter, a second flush was performed to recover the solution remaining in the uterus. Animals from the control group were subjected to a single uterine flush. From 210 double-flushing procedures, 1409 viable embryos were recovered. In comparison, from 432 cows receiving the single-flushing procedure, 1993 embryos were recovered. Double flushing increased (P < 0.05) the number of embryos recovered per procedure compared to single flushing (6.7 +/- 0.4 versus 4.6 +/- 0.2, respectively; mean +/- S.E.M.). When double flushing was performed, average recovered embryos/ova increased (P < 0.05) from 8.3 +/- 0.4 to 12.7 +/- 0.7 in Limousin and from 7.9 to 11.5 in Guzera. Also, utilization of double flushing increased (P < 0.05) the number of viable embryos from 4.7 +/- 0.3 to 6.9 +/- 0.5 in Limousin and from 4.5 +/- 0.4 to 6.4 +/- 0.7 in Guzera. Mean total embryos/ova was similar (P > 0.05) between the control group and after the first uterine flushing in the double-flushing group; therefore, both flushings were conducted efficiently. In conclusion, double uterine flushing increased embryo recovery in cattle.

Animals↗
PubMed2004

Genotoxicity of hormonal steroids.

Hormonal steroids have a widespread use in medicine and their side effects are continuously debated. The possible genotoxic activity of steroids has been the subject of many investigations. The natural estrogens estradiol, estrone and estriol are generally negative in the ICH core battery of tests, but several positive results have been obtained when using additional endpoints of genotoxicity. The genotoxic activity of the 4-hydroxy metabolites of estradiol and estrone is well established. The synthetic steroidal estrogens have a comparable profile of negative and positive test results. Cyproterone acetate and some of its analogues have a special position within the group of progestins. Their genotoxic potential has been established. Other progestins are generally negative in the routine tests. Anti-glucocorticoids, anti-progestins, corticosteroids, androgens, anabolics and anti-androgens appear to be devoid of genotoxic activities. The genotoxic potential of estradiol, estrone and cyproterone acetate with its analogues may play no role under normal physiological and therapeutic conditions. The metabolic conditions that are needed for the formation of DNA-reactive metabolites and oxygen radicals may not be present in humans. Epidemiological cancer data seem to support this view. The importance of thresholds in the dose-effect-relationship of genotoxicity data and their use in risk assessment is discussed.

Androgens↗
PubMed2002

Atherosclerosis imaging methods: assessing cardiovascular disease and evaluating the role of estrogen in the prevention of atherosclerosis.

Various interventions for cardiovascular disease (CVD) slow or reverse the progression of atherosclerosis and reduce the risk of clinical coronary events. Although the cardiovascular benefits of hormone replacement therapy have been demonstrated in observational studies in predominantly healthy women, no benefit has been found in a randomized clinical trial conducted in older women with established CVD. It is possible that the benefit of hormone therapy occurs when it is used relatively early in the progression of atherosclerosis. Techniques are now available to monitor the various stages of atherosclerosis. Quantitative coronary angiography, a technique used to evaluate relatively late-stage atherosclerosis, has been shown to predict the risk of subsequent clinical coronary events. B-mode ultrasonography of the intima-media wall thickness (IMT) of the carotid artery can assess the earlier stages of atherosclerosis and correlates with atherosclerosis risk factors, as well as with clinical cardiovascular and cerebrovascular outcome. This technique offers a relatively rapid and cost-effective method to test therapies for CVD and to screen for individuals who are at high risk for cardiovascular events. As an example of the use of atherosclerosis imaging to evaluate possible therapeutic interventions, measurements of IMT were performed in a randomized, controlled trial comparing oral 17beta-estradiol with placebo. The results demonstrated that 17beta-estradiol significantly reduces the progression of subclinical atherosclerosis in healthy, postmenopausal women when compared with placebo.

Coronary Angiography↗
PubMed1993

Diagnosis and management of extrauterine pregnancies.

This study was based on 16 women provisionally diagnosed as having extrauterine pregnancies. Of these, 13 (81.3%) were confirmed as positive at operation. Patients were managed according to 1 of 3 regimens; 1) methotrexate (n = 4), 2) methotrexate followed by surgery (n = 3) and 3) surgery (n = 6). Serial blood samples, collected before and after treatment, were analyzed for ovarian (oestradiol, E2; progesterone, P4) uterine (placental protein 14, PP14) and placental markers (chorionic gonadotrophin, HCG; pregnancy-associated plasma protein-A (PAPP-A). Of the pretreatment samples, only 30.4% and 41.7% were depressed for PP14 and HCG, respectively. By contrast, the diagnostic value of PAPP-A (77.8%) and P4 (87.5%) was greater. Biochemical monitoring of treatment was best achieved with trophoblastic derived antigens (HCG), whereas antigens of maternal origin demonstrated widely varied responses. This study established the effectiveness of chemotherapy for treatment of tubal pregnancies as an alternative to surgery, but if a biochemical marker is required, the marker of choice is HCG.

Abortion, Therapeutic↗