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PubMed1989

In vitro biotransformation of estradiol by explant cultures of murine mammary tissues.

In vivo experiments have demonstrated a correlation between the extent of 16 alpha-hydroxylation of estradiol and incidence of mammary cancer. The ability of mammary ductal epithelium (MDE), the site for neoplastic transformation, to metabolize estradiol or to accumulate estradiol metabolites has not been unequivocally established. Using a newly developed mammary explant culture system and a radiometric assay, we have compared the site-specific metabolism of estradiol (E2) by the C-17-oxidation and C-16 alpha-hydroxylation pathways in mouse tissues that differ in relative risk for mammary cancer. A comparison between MDE (target tissue) and liver (nontarget tissue) from NFS (low risk) and C3H/ouj (high risk) mice revealed that: a) increase in C-17-oxidation was similar in MDE and liver from the two strains, and b) while C-16 alpha-hydroxylation was similar in liver from the two strains (p = 0.5, n.s.), it was increased 4-fold in the MDE from the high risk C3H/ouj strain relative to that from the low risk NFS strain (p = 0.001). Furthermore, in vivo administration of progesterone resulted in modulation of cell proliferation as well as of E2 metabolism in mammary explant cultures. The effect of progesterone depended upon the presence of the MtV-2 proviral gene. This study demonstrates that mammary explants can extrahepatically metabolize estradiol. The specific risk-related increase in C-16 alpha-hydroxylation suggests that intrinsic metabolic ability of the target tissue leading to the formation of 16 alpha-hydroxyestrone from estradiol may be a determinant in the relative risk for developing mammary cancer.

Animals↗
PubMed1991

Inhibition of T47D human breast cancer cell growth by the synthetic progestin R5020: effects of serum, estradiol, insulin, and EGF.

The mechanism of the antiproliferative effects of progestins on human breast cancer cells is not known. In view of the ability of estrogen to stimulate human breast cancer cell production of peptide growth factors, and since previous studies have suggested that the inhibitory action of progestins is dependent on estrogen-stimulated growth, the present study examined the interaction of growth factors and the synthetic progestin R5020 on the proliferation of T47D human breast cancer cells. In this study, the concentrations of estradiol, insulin, and EGF for optimal stimulation of T47D cell growth in 3% dextran-charcoal treated fetal bovine serum (DCC-FBS) were determined to be 1 nM, 100 nM, and 1 nM, respectively. Furthermore, incubation with these optimal concentrations of estradiol, insulin, and EGF in various combinations produced additive effects on T47D cell proliferation, suggesting that these agents act, at least in part, by different mechanisms. In contrast, in a chemically defined medium (DM), both estradiol and EGF were unable to stimulate T47D cell proliferation. In the case of estradiol, the inability to demonstrate stimulation of T47D cell growth in DM was not due to down-regulation of the estrogen receptor. R5020 inhibited the growth of T47D cells, although its effect was more marked in the presence of 3% DCC-FBS than in DM. Stimulation of T47D cell growth by either estradiol or insulin in 3% DCC-FBS was effectively inhibited by R5020. In contrast, growth of T47D cells stimulated by EGF in the absence of estradiol was not markedly inhibited by R5020, the growth being comparable to that of untreated control cells. These findings suggest that the inhibitory effect of R5020 on T47D cell proliferation is dominant over the action of some, but not all, breast cancer mitogens.

Animals↗
PubMed1986

Estrone sulfate: a potential source of estradiol in human breast cancer tissues.

Local formation of estradiol in human breast tumors could provide a more important source of estrogen than is delivered from plasma. Prior studies have suggested that estrone is primarily synthesized from estrone sulfate. The enzyme 17 beta-hydroxysteroid dehydrogenase (HSD) would be required to convert estrone to estradiol. This study characterized HSD in 1000 X g supernatants from human breast tumors. Estradiol synthesis was linearly related to tissue concentration or time over the range studied. Cofactor requirements varied with estrone concentration. High and low affinity sites were found in 50% of tissues studied, while the remainder contained only low affinity sites. Screen assays showed measurable activity in all 42 samples tested. This activity ranged from 0.73- greater than 100 nmol estrone synthesized/g protein/hr, with a median activity of 5.9 nmol/g/hr. We evaluated the biological relevance of the sulfatase-HSD pathway by testing the ability of estrone sulfate to stimulate colony formation in soft agar cultures of nitrosomethylurea-induced rat mammary tumors. The maximally effective concentration ranged from 10(-7) to 10(-4)M. Significant stimulation of colony formation was observed in 7 of 8 experiments. The estrone sulfate stimulation pattern was similar to that previously observed with estradiol. Of the 3H-estrone sulfate added to the dishes, 20-98% was recovered as estrone and 0.2-6% as estradiol. These studies suggest that the requisite enzymes are present in human breast tumors for conversion of estrone sulfate to estradiol, and that this pathway may be biologically significant.

17-Hydroxysteroid Dehydrogenases↗
PubMed1995

Thrombospondin co-localises with TGF beta and IGF-I in the extracellular matrix of human osteoblast-like cells and is modulated by 17 beta estradiol.

Thrombospondin (TSP) is a multifunctional glycoprotein which is synthesised by several cell types including osteoblasts, and incorporated into the extracellular matrix (ECM) of these cells. The function and regulation of TSP in bone is not clear. In this study, using a long term culture model of human osteoblast-like cells, we examined the distribution of TSP in the ECM and its modulation by added estradiol. In this model the osteoblast-like cells form a regular multilayer which continues to increase in depth up to 50 days post confluence. In the ECM of these cultures and in 19-week fetal bone, the bone markers osteocalcin and alkaline phosphatase were diffusely distributed in the matrix. In contrast, labelling for TSP was concentrated, confined to the banded collagen and its immediately adjacent ECM. This pattern of labelling resembled that of the growth factors transforming growth factor beta-I (TGF beta), and insulin-like growth factor-I (IGF-I), with which TSP label co-localised. Labelling intensities were comparable between fetal bone and the in vitro material for TSP, TGF beta and IGF-I. TSP label was present by 10 days post confluence, reached a maximum by 20 days, and declined slowly thereafter, a time course which was similar to that of IGF-I. Incubation of osteoblast-like cell cultures with 17 beta estradiol resulted in an increase in multilayer depth and a maximal 3-fold increase in TSP labeling at 30 days as well as approximately 2-fold increases for TGF beta and IGF-I. The dose-response relationship for these responses to estradiol treatment was biphasic with maximal increases at 10(-10) M-10(-11) M of added estradiol. Treatment with 17 alpha estradiol produced labelling intensities that were not significantly different from controls. Studies with other cell types have suggested that TSP may be involved in modulation of growth factor activity. The similarities between TSP, TGF beta and IGF-I, in terms of their distribution and regulation by 17 beta estradiol treatment, may indicate a role for TSP in modulating bone cell proliferation and function through interaction with local growth factors.

Alkaline Phosphatase↗
PubMed1994

Estradiol-17 beta stimulates proliferation of uterine epithelial cells cultured with stromal cells but not cultured separately.

There is indirect evidence that the in vivo proliferative response of rodent uterine epithelium to estrogen requires interaction with the underlying stroma in pre- and post-pubescent animals. To examine this potential requirement directly, the proliferative response of epithelium to 17 beta-estradiol in the presence or absence of stroma was measured in vitro. Uterine epithelial and stromal cells were isolated separately from immature or adult mice, and were maintained as monocultures or cocultures in defined, serum-free medium with or without 8 x 10(-9) M 17 beta-estradiol. Incorporation of bromodeoxyuridine into the DNA was determined by immunolabeling to assay proliferation in individual cells. Cell morphology and immunolabeling of cytokeratin were used to distinguish epithelial from stromal cells. Treatment of cocultures with 17 beta-estradiol for 24 h increased the proliferation of epithelial cells relative to controls approximately threefold, whereas, in monocultures of epithelial or stromal cells 17 beta-estradiol decreased the number of bromodeoxyuridine-incorporating cells by approximately half. Furthermore, cell contact between epithelial and stromal cells was important for the effects of 17 beta-estradiol on cells in cocultures. Approximately three quarters of the 17 beta-estradiol-induced proliferation of epithelial cells in cocultures was produced by epithelial cells within colonies that were also contacting stromal cells. These results are consistent with the hypothesis that stromal cells mediate the estrogenic proliferative response, and provide evidence that this mediation involves cell contact or stroma-mediated changes in the microenvironment immediately around the epithelial cell.

Animals↗
PubMed1989

Estradiol receptors in the cytosol of peripheral blood mononuclear cells in hepatitis B virus carriers treated with interferon-alpha.

Estradiol receptors in the cytosol of peripheral blood mononuclear cells and the effects of interferon-alpha (IFN-alpha) on estradiol receptors were studied in asymptomatic hepatitis B virus (HBV) carriers, patients with chronic hepatitis B and normal controls. The level of estradiol receptors in the cytosol of mononuclear cells was significantly lower in asymptomatic HBV carriers and patients with chronic hepatitis B, compared to normal controls. This low level of cytosol estradiol receptors in patients with chronic hepatitis B was increased by the administration of IFN-alpha. In addition, when peripheral blood mononuclear cells from patients with chronic hepatitis B were incubated with IFN-alpha in vitro, the level of cytosol estradiol receptors also increased by increasing the concentration of IFN-alpha. We previously reported that the response of mononuclear cells to estrogen is impaired in HBV carriers, and our present results suggested that this may be due to the low level of estradiol receptors in the cytosol of mononuclear cells.

Carrier State↗
PubMed2003

Effects of estradiol and tamoxifen on proliferation of human breast cancer cells and human endometrial cells.

The effects of estradiol and tamoxifen on the proliferation of estrogen receptor positive cells and the relationship between the tamoxifen tolerance and cell origin were investigated. The tissues of human endometrium and breast cancer were randomly selected following dissection for primary cell culture. After the breast cancer cells and endometrial cells were treated with 1 x 10(-8) mol/L estradiol and/or 1 x 10(-6) tamoxifen, 3H-labelled thymine nucleotide was used to trace the kinetics of cell proliferation. There was no significant difference in the inhibition on the human endometrial cells between tamoxifen-treated group (6.3%) and control group (6.4%), but tamoxifen could significantly inhibit the proliferation of the human breast cancer cells (45.84%) as compared with control group (52.72%). Moreover, tamoxifen could significantly stimulate the proliferation of tamoxifen resistant breast cancer cells (9.64%) as compared with control group (6.32%). Estradiol could significantly stimulate the proliferation of all the three kinds of cells as compare with control group. The combined use of estradiol and tamoxifen could inhibit the proliferation of the endometrial cells and breast cancer cells as compared with estradiol used alone, but on the tamoxifen resistant breast cancer cells, they could more significantly stimulate the proliferation than E2. It was concluded that E2 could stimulate the proliferation of these three kinds of cells. However, the inhibitive effects of tamoxifen on the proliferation of these cells were dependent on the estradiol.

Adult↗
PubMed2001

Effect of 17 beta-estradiol on the brain damage and metabolic changes in rats.

An in vivo model of glutamate excitotoxicity in which glutamate is applied to the cortex of rats through a microdialysis probe has been used to investigate the neuroprotective processes initiated by 17 beta-estradiol. Rats were pre-treated with 17 beta-estradiol i.v. before local application of glutamate. The experimental results showed that pre-treatment with 17 beta-estradiol significantly reduced the size of the glutamate-induced lesion. In the microdialysates, the peak of lactate observed immediately after glutamate application was significantly higher and longer lasting after 17 beta-estradiol pre-treatment. The level of extracellular glucose was markedly decreased concomitantly to the increase in lactate, but no difference could be observed with and without 17 beta-estradiol pre-treatment. These suggest a new neuroprotective mechanism of 17 beta-estradiol by activating glutamate-induced lactate production. This effect on lactate production and lesion reduction is estrogen receptor dependent and is abolished totally by estrogen antagonist tamoxifen. It was also demonstrated here that high lactate subserves estrogen neuroprotection during glutamate toxicity.

Animals↗
PubMedDate not supplied

Transdermal 17 beta-estradiol combined with oral progestogen increases plasma levels of insulin-like growth factor-I in postmenopausal women.

In order to evaluate the effect of postmenopausal estrogen replacement therapy on the plasma levels of the insulin-like growth factor-I (IGF-I) 12 postmenopausal women aged 44 to 59 years were studied. The control group consisted of 15 healthy premenopausal women aged 20-44 years. In the postmenopausal women the plasma levels of IGF-I, gonadotrophins and sex hormones were determined before and after 3 and 6 months cyclic replacement therapy with transdermal 17 beta-estradiol (E2 100 micrograms patches applied twice weekly) combined with oral chlormadinone acetate (2 mg daily for 7 days in each cycle). Basal levels of estradiol (E2), IGF-I, dehydroepiandrosterone sulphate (DHEA-S), testosterone and androstenedione were lower, but gonadotropin levels were higher in postmenopausal than in premenopausal women. In all the women studied age was inversely correlated with IGF-I levels (r = -0.793, p less than 0.001) and with DHEA-S concentrations (r = -0.435, p less than 0.02). In postmenopausal women transdermal estradiol administration restored the circulating E2 levels to the early follicular range and increased the IGF-I levels (from 76.4 +/- 9.2 micrograms/l to 141.8 +/- 20.8 micrograms/l; p less than 0.01). Transdermal estradiol decreased gonadotrophin levels without changes in concentration of DHEA-S, testosterone, androstenedione and SHBG. In postmenopausal women before and during replacement therapy a positive correlation was found between estradiol and IGF-I concentrations (r = -0.439, p less than 0.01). These results suggest that cyclic replacement therapy with transdermal 17 beta-estradiol in combination with chlormadinone acetate given orally increase the plasma levels of IGF-I in postmenopausal women.

Administration, Cutaneous↗
PubMed2001

Modulation induced by estradiol in the acute phase of Trypanosoma cruzi infection in mice.

We investigated the effect of 17beta-estradiol on mice resistant to infection by Trypanosoma cruzi. Infected Balb/C, C3H and C57BL/6 female mice had a longer survival time than males, C57BL/6 showing the highest difference (50% cumulative mortality in females versus 100% in males). This lineage was treated with estradiol (from 0.05 microg to 500 microg/mouse) 1 day before infection. Treatment with 50 microg or 500 microg estradiol/ mouse increased mortality and parasitaemia. Low doses had no effect or tended to reduce both parameters. Given that estradiol presented no in vitro effect on trypomastigotes or epimastigotes, the involvement of a direct hormonal effect on the parasite is improbable. Alterations in the humoral T. cruzi-specific response were also discarded, since the kinetics and concentration of anti-T. cruzi IgG were not affected by the treatment. Females infected during an estradiol-descending phase (meta-oestrus) survived longer than those infected during other phases of the oestrous cycle. We confirmed that estradiol interferes with T. cruzi infection.

Acute Disease↗
PubMed2005

Effects of estradiol and dihydrotestosterone on osteoblast gene expression in osteopenic ovariectomized rats.

Because androgens increase bone formation and estrogens inhibit bone resorption, there is a potential therapeutic use for a combined treatment of these hormones to preserve bone. We investigated the effect of dihydrotestosterone (DHT) and estradiol, alone and in combination, on the mRNA levels of genes expressed during osteoblast development in osteopenic ovariectomized (ovx) rats: 40 animals were ovx and administered vehicle or 80 mg/kg body weight DHT at 15 weeks postovariectomy. At 19 weeks postovariectomy, the rats were administered vehicle or 20 mg/kg body weight estradiol for 1 week. The treatment groups were as follows: (1) vehicle + vehicle, (2) DHT + vehicle, (3) vehicle + estradiol, and (4) DHT + estradiol. Fasting blood and urine samples were collected at 15, 17, 19, and 20 weeks postovariectomy for bone biochemical analyses. On completion of both procedures, the long bones were removed and total RNA extracted. Combined DHT and estradiol treatment increased the mRNA (P < 0.001) and serum levels of alkaline phosphatase (ALP) (P < 0.01) compared to control rats. These data suggest that combined DHT and estradiol treatment stimulates osteoblasts at an early stage of their development when ALP is expressed.

Animals↗
PubMed2005

The response to sex steroid hormones and vitamin D of cultured osteoblasts derived from ovariectomized mice with and without 17beta-estradiol pretreatment.

This study investigated whether 17beta-estradiol (E2) may have different effects on osteoblasts derived from estrogen-deficient ovariectomized (OVX) mice compared to sham-operated normal animals. We studied the specific effects of 17beta-estradiol on the differentiation and function of cultured osteoblasts derived from these groups of animals, with or without estrogen replacement treatment. One-month-old mice were ovariectomized or sham-operated, and treated (every second day) for 4 weeks with 0.5 mg/kg 17beta-estradiol or with vehicle alone. At the end of the experiment, bones were removed for primary osteoblast cultures or for morphological and chemical evaluation. In cells from untreated OVX animals, alkaline phosphatase (ALP) specific activity was reduced, while collagen production and mineralization were unchanged when compared to cells from controls. In vivo estrogen pretreatment of the OVX mice elevated ALP activity and mineralization of the cells, while collagen production was reduced. The addition of 17beta-estradiol to the culture medium increased ALP activity, collagen production, and mineralization by all cultured osteoblasts, except in those derived from sham-operated, estrogen-pretreated mice, where these features remained unchanged. Osteocalcin production was unchanged. Addition of testosterone or 1,25(OH)2D3 to the culture medium induced changes that differed among the groups depending on the source of the cultured cells. It seems that ovariectomy in mice prior to culture affected the phenotype of the cultured osteoblasts and their response to estradiol, testosterone, and 1,25(OH)2D3, depending on whether animals were pretreated with estradiol or not. These results imply that the animal's estrogen status prior to culture can influence the response to estrogens; this finding may have important implications for hormone replacement therapy (HRT) in postmenopausal women.

Alkaline Phosphatase↗
PubMed2006

Is estradiol mandatory for an adequate follicular and embryo development? A mouse model using aromatase inhibitor (anastrozole).

BACKGROUND: Although high levels of estradiol are found in the follicular fluid, little is known about its necessity for adequate follicular growth, oocyte maturation and embryo development. Arimidex (anastrozole) is a potent aromatase inhibitor capable to induce an in-vivo milieu deprived of estradiol. This study uses a mouse model applying Arimidex to create an in-vivo system lacking of estradiol, in order to explore whether this gonadal steroid hormone is mandatory for folliculogenesis followed by normal fertilization and embryo development. METHODS: Experiment 1: Immature C57 Black female mice, aged 3-4 weeks were superovulated by 5 IU PMSG given intraperitoneally. A study group (9 mice) was concomitantly injected with 0.1 mg of Arimidex intraperitoneally given the morning day before PMSG, the morning day of PMSG injection and the following two days. The control group (8 mice) was similarly injected with normal saline. Estradiol (E2) and progesterone (P) serum levels were tested 48 hours after PMSG and the ovaries of each mouse blindly examined by a pathologist to evaluate follicular development. Experiment 2: 48 h after PMSG superovulation, hCG (7.5 IU) was injected intraperitoneally, followed by mating. The study group was treated with Arimidex 0.1 mg intraperitoneally daily from a day prior to PMSG injection to the day of sacrifice. The control group was treated similarly by normal saline. Forty-two hours after mating blood was withdrawn for E2 and P levels followed by tubal dissection. Embryos of 2-4 cells were cultured in-vitro and the development to the morula, blastocyst and hatching blastocyst stages were examined 24, 42, and 48 h later. RESULTS: Experiment 1: A significant reduction of E2 levels was achieved in the Arimidex group in comparison to control group (126.3+/-104.8 and 1910+/-960 pmol/L, respectively; p < 0.0001). Nevertheless, the two groups did not differ by the mean number of follicles (27+/-9.5 and 30.4+/-13.0) or the distribution for antral (65% and 68.4%) and pre-antral (35% and 31.6%) follicles, respectively. Experiment 2: The reduction of estradiol during follicular phase did not hamper follicular development, in-vivo fertilization and in-vitro embryo development. Similar rates of embryo development to the morula stage (90.6% and 86%), blastocyst stage (86% and 89%) and hatching blastocyst (81% and 78%) were achieved in the Arimidex group and the control group, respectively. CONCLUSIONS: Adequate folliculogenesis is independent of estrogen but is conditioned on gonadotropin stimulation. Moreover, depletion of estradiol in the vicinity of the oocyte did not impair its developmental potential, including its fertilization and development into morulae, blastocysts and hatching blastocysts.

Anastrozole↗
PubMed2005

Neuroprotection and protein damage prevention by estradiol replacement in rat hippocampal slices exposed to oxygen-glucose deprivation.

Here we investigated the effects of estradiol replacement in ovariectomized female rats using hippocampal slices exposed to oxygen-glucose deprivation (OGD). OGD induced lactate dehydrogenase (LDH) release to the incubation medium, what was assumed as a parameter of cellular death. In the estradiol-treated group the LDH release was markedly decreased by 23% as compared to the vehicle-treated group. In attempt to study a possible mechanism by which estradiol acts, we investigated some parameters of oxidative stress. In both vehicle-treated and estradiol-treated groups, OGD significantly increased the free radical production by 34% and 16%, respectively, although no significant differences on total antioxidant capacity were observed. Interestingly, estradiol replacement prevented the significant reduction in tryptophan and tyrosine contents caused by OGD observed in vehicle-treated animals. Our results show that estradiol replacement in ovariectomized female rats decreases cellular susceptibility to an ischemic-like injury and suggest a role for the hormone on protein damage prevention.

Animals↗
PubMed1978

Transfer of estradiol to human milk.

A radioimmunoassay for the measurement of estradiol in human milk is evaluated. The detection limit was found to be 25 pg. of estradiol per milliliter of milk. In milk samples collected from four lactating women during three to four months and from one pregnant and lactating woman, the concentration of estradiol was found to be below the detection limit of the assay. When six lactating women were given vaginal suppositories containing 50 or 100 mg. of estradiol, it was possible to estimate the estradiol concentration in milk. A ratio of transfer of estradiol from plasma to milk during physiologic conditions is calculated to be less than 100:10.

Estradiol↗
PubMed1981

Mechanism of luteolysis: effect of estradiol and prostaglandin F2 alpha on corpus luteum luteinizing hormone/human chorionic gonadotropin receptors and cyclic nucleotides in the rhesus monkey.

Recent studies from our laboratory suggest that estrogen-induced luteolysis in the primate may be mediated through synthesis of prostaglandin F2 alpha (PGF2 alpha). To elucidate further the mechanism of luteolysis, normally cycling rhesus monkeys received intra-corpus luteum (CL) injections of estradiol (100 microgram), PGF2 alpha (500 microgram), or the appropriate vehicles on the seventh day after the preovulatory estradiol surge. Peripheral vein blood was drawn, at 30-minute intervals for 6 hours for progesterone and luteinizing hormone (LH) assays. Five hours after intra-CL injection, the CL was excised and the LH/human chorionic gonadotropin (hCG) receptor-binding activity and cyclic guanosine monophosphate (cGMP) and cyclic adenosine monophosphate (cAMP) were measured. PGF2 alpha significantly (p < 0.05) lowered progesterone within 1 hour, while the time required for estradiol to lower progesterone significantly was 3.5 hours; there was no significant change in LH, Estradiol and PGF2 alpha significantly (p < 0.05) decreased the LH receptor-binding capacity at 5 hours, without any change in the binding affinity. Also PGF2 alpha significantly (p < 0.05) increased cGMP in the CL, while cAMP remained unchanged; estradiol treatment resulted in a significant (p < 0.05) increase in cAMP with no change in cGMP. This study suggests that estradiol and PGF alpha cause a decrease in progesterone secretion by a loss of the LH/hCG receptor and the PGF2 alpha may act further through the cGMP system.

Adenosine Monophosphate↗
PubMed1984

Does sex hormone-binding globulin play a role in the transport of estradiol in vivo?

The distribution of estradiol and testosterone into sex hormone-binding globulin (SHBG)-bound, albumin-bound, and unbound fractions in whole serum under equilibrium conditions at 37 degrees C is described in women with normal menstrual cycles, pregnant women, and newborn infants. The percentage of estradiol bound to SHBG was determined by equilibrium dialysis at 37 degrees C. Whole serum, 0.1 ml, was dialyzed against 0.1 ml of the same serum heated at 60 degrees C for 1 hour (a procedure shown to denature SHBG but not to affect albumin). The percentage of unbound estradiol in whole serum was measured by dialyzing native serum against an isosmotic dextran solution. Testosterone binding was studied similarly. Our findings show that SHBG is an important binder of estradiol in both pregnant and nonpregnant women. However, estradiol binding by SHBG is undetectable in the newborn infant. Testosterone is significantly bound to SHBG under all circumstances. We conclude that SHBG does play a role in the transport of estradiol in women, particularly in pregnancy.

Adult↗
PubMed1986

Effects of clomiphene citrate on cytosolic estradiol and progesterone receptor concentrations in secretory endometrium.

Cytosolic estradiol and progesterone receptor concentrations were measured in luteal phase endometrial biopsy samples obtained from 12 anovulatory or oligoovulatory women on clomiphene citrate therapy and from 40 normal control subjects. Clomiphene citrate treatment (250 to 750 mg per cycle) decreased both endometrial estradiol and progesterone receptor concentrations. Estradiol receptor levels were nondetectable in seven tissue samples and progesterone receptor levels in four samples from the 12 subjects given clomiphene citrate compared to nondetectable estradiol receptor concentrations in one tissue sample and progesterone receptor concentrations in two samples from the 40 normal control subjects. In histologically dated endometrium, mean estradiol receptor concentrations on days 20 to 23 and progesterone receptor levels on days to 24 to 27 were lower than the values observed in the comparable dated endometrium of normal ovulatory women. Steroid receptor concentrations correlated negatively with the duration of clomiphene citrate therapy, which implies a time-dependent suppressive effect of clomiphene citrate on measurable cytosolic estradiol and progesterone receptor concentrations during the luteal phase of the cycle.

Adult↗