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PubMed2005

Testosterone and estradiol among older men.

CONTEXT: Testosterone and estradiol levels decline with age in men. This change may affect multiple clinical outcomes, but there have been few reports of the distribution and correlates of testosterone and estradiol concentrations in elderly men. OBJECTIVE: The purpose of these studies was to assess sex steroid levels in a large cohort of older men. DESIGN: We conducted a cross-sectional cohort evaluation. SETTING: Community-dwelling men were studied at six academic medical centers in the United States. PARTICIPANTS: The Osteoporotic Fractures in Men Study is a prospective cohort of men aged at least 65 yr. In these studies, a randomly selected stratified subsample of 2623 participants was analyzed. MAIN OUTCOME MEASURES: We assessed levels of total and free testosterone and estradiol and SHBG. RESULTS: Age was inversely associated with free testosterone and free estradiol levels (P for trend = 0.001 for both). Notably, at any age, there was substantial variation in levels of each hormone. Free testosterone levels were lower in men with greater body mass index, lower SHBG, and poorer self-reported health status and in those of Asian race. Free estradiol concentrations were lower in men with lower body mass index and higher SHBG levels. Free estradiol and free testosterone were modestly correlated (r = 0.20; P < 0.001), but at any level of free testosterone, there was considerable variation in free estradiol levels. CONCLUSIONS: This is the largest cohort of older men in which sex steroid levels are available, and it demonstrates that testosterone and estradiol, and their free fractions, tend to decline with age even among older men. However, substantial variation is also present. The relationships between sex steroid levels and their consequences in aging are likely to be complex.

Aged↗
PubMed1982

Effects of human cirrhotic serum on estradiol and testosterone transport into rat brain.

It is known that sex hormone-binding globulin (SHBG), which binds both testosterone and estradiol in human serum, is markedly elevated in cirrhosis. In addition, it is known that the net metabolic clearance of testosterone is decreased in cirrhosis, while no change in the metabolic clearance of estradiol is observed. Since net clearance estimates are not direct measures of plasma protein binding effects, the present studies were designed to examine the effects of cirrhotic human serum on the unidirectional clearance of sex steroids using an in vivo rat brain paradigm previously described. Cirrhotic serum was characterized by the following changes from control serum: 2.6-fold increase in SHBG, 40% decrease in albumin, and 30% and 22% decreases in the dialyzable fractions of testosterone and estradiol, respectively. In addition, the non-SHBG-bound fraction of estradiol was decreased 41% in cirrhosis, but no significant change in the brain extraction of estradiol was observed using cirrhotic serum. In contrast, the unidirectional testosterone clearance was decreased 33% by cirrhotic serum. These studies indicate that changes in the net metabolic clearance of sex steroids closely parallel the changes in unidirectional clearance caused by alterations in plasma proteins. The absence of a decrease in estradiol clearance in cirrhosis in association with the substantial decrease in the non-SHBG-bound estradiol fraction is an unexpected finding, since previous studies have shown that a close parallel exists between these two parameters. A possible explanation is that estradiol bound to the SHBG in human cirrhotic serum is partially available for transport into peripheral tissues such as the brain.

Adult↗
PubMed1995

17 beta-estradiol stimulates prostacyclin, but not endothelin-1, production in human vascular endothelial cells.

The exact mechanisms by which estrogens protect against occlusive vascular disorders are not known. One possibility could be an effect on vascular endothelial vasoactive compounds, such as vasodilatory prostacyclin (PGI2) and vasoconstrictory endothelin (ET-1). Here we report on the effect of 17 beta-estradiol on the synthesis of PGI2 and ET-1 in cultured human umbilical vein endothelial cells. These cells were incubated in the absence (control) and presence of 17 beta-estradiol (0.001-1 mumol/L) for 3-24 h with serum (10%) or without serum. The release of PGI2, as assessed by its metabolite 6-keto-prostaglandin F1 alpha, and that of ET-1, were assessed by RIA. 17 beta-Estradiol (0.01-0.1 mumol/L) predissolved in ethanol (final concentration, 0.01%) increased PGI2 production by 26-30% in endothelial cells incubated without serum. This increase in PGI2 production was enhanced up to 66% when 17 beta-estradiol (1 mumol/L) was encapsulated within beta-cyclodextrin. The stimulation of PGI2 production was detectable after 12 h of incubation. The 17 beta-estradiol-induced stimulation of PGI2 production was blocked in dose-dependent manner by antiestrogenic tamoxifen. 17 beta-Estradiol failed to affect the production of PGI2 if the endothelial cells were incubated with serum and had no effect on ET-1 production under any conditions. 17 beta-Estradiol-induced stimulation of vasodilatory and antiaggregatory PGI2 production without a concomitant change in vasoconstrictory ET-1 production may provide one explanation for the ability of estradiol to maintain vascular health and protect against vascular disorders.

6-Ketoprostaglandin F1 alpha↗
PubMed2000

The effect of low dose micronized 17ss-estradiol on bone turnover, sex hormone levels, and side effects in older women: a randomized, double blind, placebo-controlled study.

The purpose of this study was to examine the effects of three doses (0.25, 0.5, and 1.0 mg/day) of micronized 17ss-estradiol on bone turnover, sex hormone levels, and side effects compared with placebo in healthy older women. The study design was randomized, double blind, and placebo controlled. The setting was a university clinical research center. Healthy, community-living women over 65 yr of age participated in the study. The main outcome measures were serum and urinary biochemical markers of bone resorption and formation at baseline, 6 and 12 weeks on treatment, and 6 and 12 weeks off treatment. Markers of bone resorption were N-telopeptides of type I collagen, C-telopeptides of type I collagen, and total deoxypyridinoline cross-links; formation markers were bone alkaline phosphatase, osteocalcin, and N-terminal procollagen peptides. We also measured serum estradiol, estrone, and sex hormone-binding globulin levels at baseline, 12 weeks on treatment, and 12 weeks posttreatment. All markers of bone resorption significantly decreased at 12 weeks on treatment compared with placebo and returned toward baseline at 12 weeks posttreatment. Two markers of bone formation, bone alkaline phosphatase and N-terminal procollagen peptides, significantly decreased 12 weeks posttreatment, but the decrease in osteocalcin varied with time and estrogen dose. Based on equivalence testing, the response of markers of bone turnover to therapy with 0.25 mg/day was similar to that seen with 1.0 mg/day. Serum estradiol increased compared with baseline in all treatment groups and compared with placebo in the two higher dose groups. Breast tenderness, bleeding, and endometrial changes were significantly less frequent in the 0.25 mg/day and placebo groups compared with the higher dose groups. We conclude that low dose of estrogen (0.25 mg/day 17ss-estradiol) reduced bone turnover to a similar degree as that seen with usual replacement therapy (1.0 mg/day 17ss-estradiol), but had a side effect profile similar to that of placebo. In our study additional increases in estradiol levels, as seen with 0.5 and 1.0 mg/day 17ss-estradiol treatment, resulted in more side effects without evidence of additional benefit to bone. These data suggest that 0.25 mg/day 17ss-estradiol may be an effective and tolerable agent for the treatment of osteoporosis in older women.

Aged↗
PubMed2000

Estrogen replacement therapy in a man with congenital aromatase deficiency: effects of different doses of transdermal estradiol on bone mineral density and hormonal parameters.

The effects of different doses of transdermal estradiol (TE) on bone mineral density (BMD) in a man with aromatase deficiency were evaluated. The study protocol was divided in the following four phases: phase 1, before estradiol treatment; phase 2, 50 microg TE twice weekly for 6 months; phase 3, 25 microg TE twice weekly for 9 months; and phase 4, 12.5 microg TE twice weekly for 9 months. X-rays of hands, legs, and pelvis were performed, and BMD of the lumbar spine, hormonal parameters (LH, FSH, testosterone, and estradiol), and markers of bone turnover were determined during each phase. BMD in phase 1 was 0.933 g/cm2 and increased to 1.051 and 1.173 g/cm2 after 4 and 7 months of TE, respectively. In phase 3, BMD reached the maximum value (1.275 g/cm2). In phase 4, BMD decreased to 1.180 g/cm2 and was 1.029 g/cm2 at the end of the study protocol. A bilateral necrosis of femoral heads was also detected by x-ray films. In phase 1 serum testosterone was in the normal range, whereas serum estradiol was undetectable. During the 24-month period of treatment with TE (phases 2-4), estradiol was directly related to the amount of TE, whereas LH was inversely related to estradiol serum levels. Estradiol and gonadotropins reached optimal values only in phase 3, when FSH also was near normal; serum testosterone concentrations were normal in phases 3 and 4. This study confirms the role of estrogens in achieving and maintaining bone mineral content in the human male, providing further clinical tools useful in the management of bone loss in aromatase deficiency in the male. We suggest that the adequate substitutive dose of TE for maintaining both bone mass and normal estradiol serum levels in adult men with aromatase deficiency may be 25 microg twice weekly (0.47 microg/kg weekly).

Administration, Cutaneous↗
PubMed1982

Estradiol 17 beta-sulfate as a substrate for 2-hydroxylation enzyme of rat liver microsomes (clinical analysis on steroids. XX).

4-14C-Estradiol and its 17 beta-sulfate were incubated with rat liver microsomes under NADPH-generating system. Estradiol in liver microsomes from male and female rats was metabolized to multiple kinds of oxidized products including estrone, 2-hydroxyestrone, 2-hydroxyestradiol, and other minor steroids. Incubation of estradiol 17 beta-sulfate was carried out by the same condition, and it was shown that the metabolic pattern between male and female rats was different. By incubation of estradiol 17 beta-sulfate with male rat liver microsomes, 2-hydroxyestradiol 17 beta-sulfate was obtained as the sole product (6%). The hydroxylation was shown to occur without cleavage of the conjugate group. No such regulating effect by conjugate group on 2-hydroxylation of estradiol 17 beta-sulfate was observed in liver microsomes from female rats. The amount of 2-hydroxyestradiol 17 beta-sulfate formed was only 1%, and other metabolites which were thought to be monohydroxylated estradiols were produced as the major products. The 2-hydroxylated metabolite of estradiol 17 beta-sulfate was confirmed by its isolation as a stable form of derivative by the following way. The incubation mixture of massive amount of estradiol 17 beta-sulfate was extracted with n-butanol. Methylation of the extract with diazomethane, followed by acid-catalized hydrolysis, acetylation, and finally separation by preparative thin-layer chromatography, gave a crystalline material, the spectral properties of which were completely identical with those of the synthetic specimen, 2, 3-dimethoxy-1,3,5(10)-estratrien-17 beta-yl acetate.

Animals↗
PubMed1999

Tumor necrosis factor alpha inhibition of follicle-stimulating hormone-induced granulosa cell estradiol secretion in the human does not involve reduction of cAMP secretion but inhibition at post-cAMP site(s).

Tumor necrosis factor alpha (TNF) inhibits follicle-stimulating hormone- (FSH)induced estradiol secretion by granulosa cells in several species, including humans. One major inhibitory effect of TNF in rat granulosa cells is at the level of stimulatable adenylyl cyclase, resulting in reduced cAMP concentrations. The purpose of the present study was to investigate whether a reduction in cAMP secretion could account for the inhibitory effects of TNF on FSH-induced estradiol in human granulosa cells. Granulosa cells were taken from ovaries of premenopausal women undergoing oophorectomy for reasons unrelated to ovarian pathology. Women in this study were in various stages of the menstrual cycle or exhibited irregular cycles. Granulosa cells from follicles ranging from 5 to 10 mm diameter were subjected to culture for 48 and 96 h. Granulosa cells were cultured with human FSH (2 ng/mL) and testosterone (1 microM) in the presence and absence of human TNF (20 ng/mL). Media were collected at 48 h, fresh media and hormones added, and cultures continued for an additional 48 h. Accumulation of cAMP, progesterone, and estradiol in media were determined by radioimmunoassay (RIA). FSH induced significant increases in cAMP, progesterone, and estradiol by 96 h of culture. TNF inhibited the secretion of estradiol at 96 h without reducing the accumulation of cAMP and progesterone in media. Similar results were observed in the presence of 0.1 mM isobutylmethylxanthine (D3MX), a phosphodiesterase inhibitor that would prevent metabolism of cAMP to AMP. To determine whether TNF would inhibit the ability of cAMP to induce estradiol and progesterone secretion, granulosa cells were incubated with 0.1 mM cAMP in the presence and absence of TNF. TNF consistently inhibited the ability of cAMP to increase estradiol secretion. These results indicate that a pathway for TNF inhibition of FSH- or cAMP-induced estradiol secretion in human granulosa cells is at post-cAMP sites rather than inhibition of FSH-stimulatable adenylyl cyclase.

1-Methyl-3-isobutylxanthine↗
PubMed2006

Regulation of GnRH I receptor gene expression by the GnRH agonist triptorelin, estradiol, and progesterone in the gonadotroph-derived cell line alphaT3-1.

The secretion of luteinizing hormone (LH) and the GnRH receptor (GnRH-R) concentration are modulated by ovarian steroids and GnRH. To elucidate whether this regulation is due to alterations at the transcriptional level, we examined the GnRH I-R mRNA expression in the gonadotroph-derived cell line alphaT3-1 treated with different estradiol and progesterone paradigms and the GnRH I agonist triptorelin. alphaT3-1 cells were treated with different steroid paradigms: 1 nM estradiol or 100 nM progesterone for 48 h alone or in combination. Cells were exposed to 10 nM or 100 pM triptorelin for 30 min, 3 h, 9 h, or, in pulsatile way, with a 5-min pulse per hour. The GnRH I-R mRNA was determined by Northern blot analysis. GnRH I-R mRNA from cells treated with continuous triptorelin decreased in a time- and concentration-dependent manner. Pulsatile triptorelin increased GnRH I-R gene expression. Progesterone alone further enhanced this effect, whereas estradiol and its combination with progesterone diminished it. Continuous combined treatment with estradiol and progesterone lead to a significant decrease of GnRH I-R mRNA by 30% and by 35% for estradiol alone. The addition of 10 nM triptorelin for 30 min or 3 h could not influence that steroid effect. In conclusion, estradiol and progesterone exclusively decreased GnRH I-R mRNA in alphaT3-1 cells no matter whether they are treated additionally with the GnRH I agonist triptorelin. The enhanced sensitivity of gonadotrophs and GnRH I-R upregulation by estradiol is not due to increased GnRH I gene expression because GnRH I-R mRNA is downregulated by estradiol and progesterone. Other pathways of the GnRH I-R signal transduction might be involved.

Animals↗
PubMed1994

Effect of estradiol-17 beta on basal and hCG stimulated progesterone secretion by porcine luteal cells isolated in various stages of the luteal phase.

To explore the direct effect of estradiol-17 beta on pig luteal cells and its ability to counteract a gonadotropic stimulus, luteal cells were incubated in vitro in the presence of estradiol alone, human chorionic gonadotrophin (hCG) alone or estradiol combined with hCG. Luteal cells were collected at three different stages of the luteal phase (0-3 days after ovulation, early; 8-10 days after ovulation, mid; and 14-16 days after ovulation, late). Estradiol alone did not exert any effect on progesterone production by any of the 3 types of luteal cells. Progesterone production by cells in the mid-luteal phase was enhanced by hCG in a dose dependent manner. High doses of estradiol combined with hCG significantly diminished production of progesterone by cells collected during the early luteal phase. The strongest inhibitory effect of estradiol on hCG stimulated progesterone production was observed in cultures of luteal cells in the midluteal phase. In contrast, 100 ng of estradiol and the 10 and 100 ng/ml concentrations of hCG increased progesterone secretion over basal control values in cultured luteal cells in the late luteal phase. Differences in the production of progesterone in response to estradiol at different stage of the luteal phase suggest that different cellular mechanisms must be triggered in each luteal phase investigated. These data support a physiological role for estrogen in the regulation of the pig corpus luteum during its life span in the non-fertile cycle.

Animals↗
PubMed1988

Inhibitory effects of estradiol on glycogen synthesis in primary cell cultures of human endometrium.

The effect of estradiol on glycogen synthesis was examined in a primary cell culture system of the human endometrium. Estradiol inhibited glycogen synthesis in a dose dependent manner with a minimum effective dose of 10(-9)M. Progesterone-induced glycogen synthesis was completely abolished by the simultaneous addition of estradiol. Estradiol did not affect the activity of glycogen phosphorylase in endometrial cells, but the activity of glycogen synthetase was decreased by estradiol irrespective of the presence of progesterone. The inhibitory effect of estradiol on the glycogen synthesis of endometrial cells seemed to be mediated by estradiol receptor, because LY156758, an antiestrogenic drug at receptor site, reversed the inhibitory effect of estradiol.

Adult↗
PubMed2000

Bone turnover markers and estradiol level in postmenopausal women.

It has been found recently that women with estradiol (E) levels < 5 pg/ml were more likely to suffer osteoporotic fractures. We evaluated the relationships between biomarkers of bone turnover and changes in hormone levels in early or late postmenopausal women without any replacement therapy. Follicle stimulating hormone (FSH), luteinizing hormones (LH), estradiol and serum resorption (crosslaps) and formation (osteocalcin) markers were assayed. Bone densities in the spine and femoral neck were also measured. Elevated FSH, LH and decreased estradiol in postmenopausal women were accompanied by higher osteocalcin (9.1-9.7 ng/ml) and crosslaps level (3305-3458 pmol/l) compared to premenopausal women (6.8 ng/ml and 2087 pmol/l). Bone density was lower in elderly women. A significant inverse correlation was found between estradiol and crosslaps level; FSH and LH were also correlated with bone markers. Estradiol levels < 9 pg/ml were associated with increased bone resorption, decreased hip bone density and higher frequency of osteopenia and osteoporosis. Over 57% of women with an estradiol < 9 pg/ml could be identified as having "a high turnover" compared with 30% with estradiol above 9 pg/ml. Our results indicate that changes in bone density may not be very clear but an increase in bone turnover is distinctly apparent in women with severe estradiol deficiency.

Absorptiometry, Photon↗
PubMed1989

The stimulated C-kinase activity in estradiol-treated rat pituitaries is reduced by chronic treatment with the dopamine agonist CV 205-502.

To investigate whether the modulation of lactotrope cell multiplication and prolactin secretion in rat pituitary glands implicated the phosphoinositide C-kinase system, female Wistar rats were treated or not-with the dopamine agonist CV 205-502 or 8 days or with estradiol cervical implants for 8 for 15 days, alone or in combination with CV 205-502 for the last 8 days. CV 205-502 treatment induced a significant reduction in plasma PRL levels and in pituitary weights, whereas estradiol treatment induced a significant increase in both parameters. CV 205-502, in association with estradiol, counteracted estradiol stimulation of PRL levels and of pituitary weights. Total C-kinase activity in controls was 29.8 +/- 9.9 pmol 32phosphorus/min (N = 7, mean +/- SEM), mainly found in the soluble fraction (84%). When administered alone, CV 205-502 induced a significant reduction (-58%, p less than 0.02) in C-kinase activity in the particulate fraction with no modification in the soluble fraction. Both 8 and 15 days estradiol treatment induced a significant stimulation of total C-kinase activity, 74% and 155% respectively. When combined with estradiol, CV 205-502 significantly (p less than 0.02) counteracted the estradiol increase in total C-kinase activity, which was only 45% over control values. We conclude that treatment with a dopamine agonist and estradiol, which have antagonistic effects on the pituitary, exerts an opposite regulation of C-kinase activity. Whether this may be one of the mechanisms involved in their interaction on pituitary lactotropes remains to be determined.

1-Phosphatidylinositol 4-Kinase↗
PubMed2002

Comparative activity of pulsed or continuous estradiol exposure on gene expression and proliferation of normal and tumoral human breast cells.

Intranasal administration of hormone replacement therapy presents an original plasma kinetic profile with transient estrogen levels giving rise to the concept of pulsed therapy. To further understand the molecular effects of this new therapy, we have compared the effects of pulsed and continuous estradiol treatments on two critical aspects of estradiol action: gene expression and cell proliferation. Cells were stimulated with estradiol as 1-h pulsed or 24-h continuous treatments at concentrations such that the 24-h exposure (concentration x time) was identical in both conditions. In MCF7 cells, the transcriptional activity of estrogen receptors (ER) on a transiently transfected responsive estrogen response element-luciferase reporter construct was shown to be drastically (approximately 10-fold) and similarly stimulated after both treatments. Moreover, the increased mRNA expression of three representative estradiol-sensitive genes (pS2, cathepsin D, progesterone receptor), evaluated by Northern blot, was identical after 1-h pulse with 7 nM estradiol or continuous treatment with 0.29 nM estradiol with the same kinetic profile over 48 h. Proliferation was quantified by a histomorphometric method on primary cultures of human normal breast cells from reduction mammoplasties and using a fluorescence DNA assay in six human breast cancer cell lines which were ER positive or negative. After a 7-day treatment period, estradiol had no effect on the proliferation of the three ER negative cell lines (BT20, MDA MB231, SK BR3) but significantly stimulated the proliferation of the normal cells and of the three tumoral hormone-sensitive cell lines (MCF7, T47D, ZR 75-1); both hormone treatments producing the same increases in cell growth. In conclusion, we have shown that the genomic or proliferative effects of estradiol were identical with pulsed or continuous treatments, thus indicating that estrogenic effects are not strictly related to concentrations but rather to total hormone exposure.

Administration, Intranasal↗
PubMed2005

Effect of 17beta-estradiol on tumor necrosis factor-alpha-induced cytotoxicity in the human peripheral T lymphocytes.

We determined the effect of 17beta-estradiol on tumor necrosis factor alpha (TNF-alpha)-induced cytotoxicity in human peripheral T lymphocytes (T cells) using lactate dehydrogenase assay. Treatment with 17beta-estradiol (1-100 nM) for 24 h showed dose-dependent reduction of TNF-alpha-induced cytotoxicity in T cells. To further evaluate the mechanism of 17beta-estradiol on TNF-alpha-induced cytotoxicity in T cells, we identified estrogen receptor (ER) protein in T cells using immunocytochemistry and used the pure ER antagonist ICI 172,780. ERalpha immunoreactivity was clearly observed in T cells. ERbeta immunoreactivity was also detected in some T cells. ICI 172,780 (10(-7) M) alone did not affect cytotoxicity in T cells, however, ICI 172,780 (10(-7) M) completely abolished 17beta-estradiol cytoprotective effects in T cells. TNF-alpha tended to increase nuclear factor kappaB (NF-kappaB) protein levels in nuclear extracts but it did not reach statistical significance by Western blotting. In contrast, NF-kappaB protein levels in nuclear extracts followed by TNF-alpha with 17beta-estradiol treatment were significantly increased compared with NF-kappaB protein levels in untreated group. NF-kappaB blocker pyrrolidinedithiocarbamate (PDTC) (10(-4) M) alone did not affect cytotoxicity in T cells. In contrast, PDTC (10(-4) M) completely abolished 17beta-estradiol cytoprotective effects in T cells. Caspase -3/-7 activity was significantly increased followed by TNF-alpha, and 17beta-estradiol treatment significantly reduced the increment. The present studies suggest the protective effect of 17beta-estradiol on TNF-alpha-induced cytotoxicity through ERs in T cells and that NF-kappaB activation and caspase suppression may be involved in the mechanism.

Adult↗
PubMed2006

Sorption and transport of 17beta-estradiol and testosterone in undisturbed soil columns.

Land-applied domestic animal wastes contain appreciable amounts of 17beta-estradiol (henceforth, estradiol) and testosterone. These sex hormones may be transported through soil to groundwater and streams, where they may adversely affect the environment. Previous column transport studies with these hormones used repacked soil and did not consider preferential flow. We, therefore, determined the sorption and transport characteristics of estradiol and testosterone in undisturbed soil columns (15-cm i.d. by 32-cm height). In the sorption experiment, isotherms for estradiol and testosterone were nonlinear with Freundlich exponents (n) less than one. Sorption of both hormones decreased with soil depth, and estradiol sorbed more strongly than testosterone. Average estradiol Freundlich sorption coefficients (K(f)) values were 36.9 microg(1 - n) mL(n) g(-1) for the 0- to 10-cm soil depth and 25.7 microg(1 - n) mL(n) g(-1) for the 20- to 30-cm soil depth. Average testosterone K(f) values were 26.7 microg(1 - n) mL(n) g(-1) for the 0- to 10-cm soil depth and 14.0 microg(1 - n) mL(n) g(-1) for the 20- to 30-cm soil depth. In the transport experiment, 27% of the estradiol and 42% of the testosterone leached through the soil columns. Approximately 50% of the remaining soil-bound hormones were sorbed in the top 10 cm of soil. In almost all instances, breakthrough concentrations of estradiol, testosterone, and a chloride tracer peaked simultaneously. Simultaneous breakthrough and HYDRUS-1D transport parameters indicated both chemical and physical nonequilibrium processes affected hormone transport. This suggests hormones placed on soil surfaces may contaminate groundwater under conditions of preferential flow.

Adsorption↗
PubMedDate not supplied

Transdermal estradiol. A review of its pharmacological profile, and therapeutic potential in the prevention of postmenopausal osteoporosis.

The estradiol transdermal therapeutic system is a percutaneous delivery device which, when affixed to the skin, delivers estradiol (the major estrogen in premenopausal women) into the systemic circulation at a constant rate for up to 4 days. Because this method of delivery avoids first-pass hepatic metabolism, premenopausal levels of estradiol can be maintained in postmenopausal women using very low dosages. Bone density decreases at an accelerated rate after the menopause, which can lead to development of osteoporosis and increased fracture risk. In common with other estrogen therapies, transdermal estradiol provides protection against osteoporosis following spontaneous or surgical menopause, as evidenced by both biochemical markers of bone resorption and, in a small number of studies, measurement of bone mineral density. Protection against further vertebral fractures was also demonstrated in women with established osteoporosis in one study. Transdermal estradiol also has beneficial effects on vaginal cytology and menopausal symptoms similar to those of oral estrogens. The tolerability of transdermal estradiol appears to be very good, the most common adverse effect being local irritation at the application site. As with other estrogens, transdermal estradiol can be given continuously or in 4-week (3 weeks on/1 week off) cycles, and concomitant progestogen therapy is recommended in women with intact uteri, in order to minimise the risk of endometrial hyperplasia. Available evidence thus suggests that transdermal estradiol may represent an attractive alternative to other forms of estrogen therapy for the prevention, and possibly treatment, of postmenopausal osteoporosis.

Administration, Cutaneous↗
PubMed1984

Production of estradiol by each ovary during the estrous cycle of cows.

The objective of our experiment was to examine changes in serum concentrations of estradiol in each utero-ovarian vein before, during and after gonadotropin surges. Four cows were given prostaglandin F2 alpha (PGF2 alpha) during diestrus and three cows were allowed to cycle spontaneously. All cows had a cannula in each utero-ovarian vein and in one jugular vein. Most cows had two transient rises in estradiol, primarily coming from a single ovary, preceding and after luteinizing hormone (LH) surges. The first rise in estradiol began after luteal regression and was sustained from 48 h before a pre-ovulatory LH surge to the end of the LH surge. The second rise in estradiol was sustained from 72 to 168 h after the end of an LH surge. To determine how rapidly asymmetrical production of estradiol began during luteolysis, several cows were injected with PGF2 alpha during the luteal phase. Blood samples were taken from a jugular and both utero-ovarian veins at hourly intervals before and after PGF2 alpha. Asymmetrical production of estradiol began within 3 h after an injection of PGF2 alpha. We concluded: (1) that a single ovary was responsible for the sustained increases in concentration of estradiol that occur during proestrus to estrus and early diestrus in cows and (2) that cows may have at least one follicle capable of producing estradiol during most days of an estrous cycle, thus little delay in selection of which follicle eventually ovulates occurs after luteal regression.

Animals↗
PubMed1998

Effects of estradiol and an aromatase inhibitor on progesterone production in human cultured luteal cells.

The human corpus luteum produces both estradiol and progesterone. It is well known that there are both autocrine and paracrine systems for the regulation of the corpus luteum and that estradiol regulates the progesterone production of the corpora lutea of some other species. To assess the direct effects of estrogen on human luteal function, we performed cell culture experiments. A low concentration of estradiol, almost equal to the amount of estradiol produced by human cultured luteal cells, directly stimulated progesterone production. 4-Cyclohexylaniline, an aromatase inhibitor, significantly reduced both progesterone production and estradiol production. Levels of estradiol higher than the levels that cultured human luteal cells themselves produced significantly reduced basal progesterone production and also significantly reduced human chorionic gonadotropin (hCG), forskolin and dibutyryl-cyclic AMP-stimulated progesterone production. According to these data, high doses of estradiol produced a luteolytic action which widely inhibited the steroidogenesis process. In conclusion, our results indicated that estradiol in part regulates progesterone production physiologically and blocks progesterone production in a pharmacological or pathological state in the human corpus luteum.

Aniline Compounds↗