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PubMedDate not supplied

Efficacy and safety of a seven-day, transdermal estradiol drug-delivery system: comparison with conjugated estrogens and placebo. The Transdermal Estradiol Patch Study Group.

OBJECTIVE: To evaluate the efficacy and safety of a new, seven-day, transdermal estradiol system in healthy postmenopausal women with hot flushes. METHODS: Two studies are described. In the first study, subjects were randomized to treatment with a 0.05 mg/day estradiol patch, a 0.1 mg/day estradiol patch, or a placebo patch; and in the second study, to treatment with either of the two estradiol patches or oral conjugated estrogens (as Premarin) 0.625 mg/day. Efficacy was evaluated on the basis of diary entries recording hot-flush frequency and severity. Subjects' and investigators' global assessments of treatment efficacy were recorded at follow-up visits. RESULTS: In Study 1, both the 0.05-mg and 0.1-mg estradiol patches were significantly more effective than placebo in reducing hot flushes and were associated with higher global assessments. In Study 2, all three active treatments produced a significant reduction in the number of hot flushes compared with base-line. There were no statistically significant between-group differences, although the response to the 0.1-mg estradiol patch was greater, and to the 0.05-mg estradiol patch less, than the response to conjugated estrogens. The patches were generally well tolerated. Skin irritation from the patch was the most common adverse experience in both studies. CONCLUSIONS: The new, seven-day, transdermal system effectively and safely treats post-menopausal vasomotor symptoms.

Administration, Cutaneous↗

PubMed1996

Serum Estradiol and Estrone Levels During 3 Weeks of Alternate-Site and Same-Site Applications of a Once-A-Week Drug-in-Adhesive Transdermal Estradiol Patch.

This open-label, randomized crossover trial was conducted in healthy postmenopausal women to characterize the serum estradiol and estrone profiles from a once-a-week transdermal estradiol patch applied repeatedly to the same site or to alternate sites on the abdomen over a 3-week period. Similar mean serum estradiol and estrone profiles and circulating estradiol:estrone ratios of approximately 1.0 were observed for both patch application regimes. Repeated application to the same or alternate sites did not result in an accumulation of exogenous estradiol or in a statistically significant increase in application-site reactions. Although the once-a-week transdermal estradiol patch should be applied to alternate sites to reduce the likelihood of dermatologic reactions, accidental application site overlap should not result in an increase in serum estradiol and estrone concentrations.

Journal Article↗

PubMed1985

Immunocytochemical evidence for endogenous calcitonin and parathyroid hormone in osteoblasts from the calvaria of neonatal mice. Absence of endogenous estradiol and estradiol receptors.

Immunoreactivities to endogenous calcitonin, endogenous parathyroid hormone, endogenous estradiol and estradiol receptors were studied in osteoblasts from the calvaria of neonatal mice by immunocytochemistry with the use of ultrathin sections obtained by cryo-ultramicrotomy. Tissues were fixed in glutaraldehyde, postfixed in osmium tetroxide and frozen in liquid nitrogen. Estradiol and estradiol receptors could not be detected in osteoblasts, whereas calcitonin- and parathyroid hormone-like immunoreactivities were observed in this cell type. Calcitonin and parathyroid hormone had similar subcellular localizations: immunoreactivities were observed at the plasma-membrane level, in the cytoplasmic matrix, and in the nucleus. These results provide immunocytological evidence for: 1) the internalization of calcitonin and parathyroid hormone in osteoblasts; 2) a direct participation of calcitonin and parathyroid hormone in the regulation of osteoblasts; 3) the absence of estradiol receptors and estradiol in osteoblasts.

Animals↗

PubMed2006

Comparison of the effects of a new conjugated oral estrogen, estradiol-3beta-glucoside, with oral micronized 17beta-estradiol in postmenopausal women.

The objective of this article is to evaluate the pharmacokinetics of serum estrone and estradiol levels in women who were taking either 17beta-estradiol-3beta-glucoside (E(2)-3beta-glucoside) or 17beta-estradiol (E(2)) daily and to examine the effects of E(2)-3beta-glucoside and E(2) on postmenopausal symptoms, gonadotropins, hepatic metabolism, and coagulation factors. Healthy postmenopausal women on estrogen who had undergone a hysterectomy were recruited. Subjects were randomly assigned to receive equivalent doses of either E(2)-3beta-glucoside or micronized E(2) for 28 days. Pharmacokinetic studies of estrone and estradiol were performed on days 1, 2, 28, and 29. Gonadotropin levels and Kupperman Index (KI) scores were determined at baseline and on treatment day 28. Mean serum estradiol and estrone concentrations in those taking E(2)-3beta-glucoside were comparable with those taking E(2). Mean baseline follicle stimulating hormone (FSH) levels were 84 +/- 27 mIU/mL and 71 +/- 24 mIU/mL in the E(2)-3beta-glucoside and E(2) groups, respectively, with significant decreases (P < 0.01) of 54 +/- 21 mIU/mL and 38 +/-18 mIU/mL, respectively, by treatment day 28. Baseline KI scores in the E(2)-3beta-glucoside group were 10 +/- 6 compared with 5 +/- 4 on treatment day 28, which is equivalent to a 50% reduction in menopausal symptoms (P = 0.003). The change in KI scores in the E(2) group was not statistically significant. Total serum estradiol and estrone levels in women taking E(2)-3beta-glucoside are comparable with those in women taking E(2). E(2)-3beta-glucoside reduces serum gonadotropin levels to the premenopausal range and is effective at reducing postmenopausal symptoms. E(2)-3beta-glucoside is a novel synthetic estrogen that is well tolerated and has promise as a hormone replacement therapy.

Administration, Oral↗

PubMed1999

A multicenter randomized comparison of cycle control and laboratory findings with oral contraceptive agents containing 100 microg levonorgestrel with 20 microg ethinyl estradiol or triphasic norethindrone with ethinyl estradiol.

OBJECTIVE: This study was undertaken to compare the effects of 2 oral contraceptive regimens on menstrual cycle control and laboratory findings. METHODS: In a multicenter randomized study 100 microg levonorgestrel with 20 microg ethinyl estradiol (Alesse or Loette) was given to 155 healthy women. A triphasic preparation of 500, 750, and 1000 microg norethindrone with 35 microg ethinyl estradiol (Ortho-Novum 7/7/7 or TriNovum) was given to 167 women for 1 to 4 cycles of treatment. RESULTS: Overall, the percentages of normal menstrual cycles and the percentages of cycles with intermenstrual and withdrawal bleeding were similar between the 2 treatment groups. In the levonorgestrel with ethinyl estradiol group, there was a statistically significantly longer latent period and a statistically significantly shorter withdrawal bleeding episode. Adverse events were similar between treatment groups, and none were serious. Most mean changes from baseline laboratory values were comparable between groups, although the mean increase in cholesterol concentration was statistically significantly lower in the levonorgestrel with ethinyl estradiol group. Changes in triglyceride and glucose concentrations were not statistically significantly different between groups. CONCLUSIONS: Levonorgestrel (100 microg) with ethinyl estradiol (20 microg) provides menstrual cycle control equivalent to that obtained with triphasic norethindrone with ethinyl estradiol (75% higher estrogen dose) with similar safety and tolerability.

Adult↗

PubMed1992

Estrogen and osteoarthritis: a study of synovial estradiol and estradiol receptor binding in human osteoarthritic knees.

Estrogen appears to be a risk factor in knee osteoarthritis (OA). Results from 21 patients revealed that synovial estradiol level was highly related to the severity of OA. Increased estradiol receptor bindings in the medial compartment of the femoral condylar and tibia plateau cartilages were observed; the increase was significantly higher in the medial than in the lateral compartment (p less than 0.05). Although the synovial estradiol level was significantly lower in women with OA than in men with OA (p less than 0.01), postmenopausal women were hypothesized to be more susceptible to OA, since the possible existence of synovial testosterone might counteract the high estradiol synovial level in men, which results in a lower incidence of knee OA in men than in postmenopausal women. We suggest that excessive synovial estradiol and higher estradiol receptor bindings may be involved in the development of knee OA, particularly in postmenopausal women.

Aged↗

PubMed1987

Interaction of two nonhistone proteins with the estradiol response element of the avian vitellogenin gene modulates the binding of estradiol-receptor complex.

The DNA sequence corresponding to the estradiol response element has been synthesized and tested in vitro for the binding of specific proteins. Gel retardation experiments combined with dimethyl sulfate protection experiments revealed that this region binds two nonhistone proteins (NHPs). One of them, NHP-1, has a molecular weight of 70,000 and binds specifically to the dyad symmetry sequence GGTCAGCGTGACC. The NHP-1 can be separated from the estradiol receptor chromatographically; it does not bind estradiol and does not cross-react with an antibody directed against the estradiol receptor. A series of synthetic "mutant" oligonucleotides were tested in a protein-DNA binding competition assay. Deletion of the GCG in the center of the dyad symmetry sequence suppressed the binding of NHP-1 by 90%, and the conversion of any GC pair to an AT pair decreased the affinity of the binding site for NHP-1. Methylation of the two CpGs on both strands of the dyad symmetry sequence decreased the affinity of the binding site for NHP-1 by 60%, whereas hemimethylation of the same structure did not inhibit the binding of NHP-1. NHP-1 and NHP-2, the NHP binding to the DNA next to the dyad symmetry sequence, bind exclusively to double-stranded DNA. NHP-2 has a molecular weight of 60,000. NHP-1 and NHP-2 are neither tissue nor species specific. In vitro reconstitution experiments show that NHP-1 and NHP-2 increase the binding efficiency of the estradiol-receptor complex to the estradiol response element.

Animals↗

PubMed1987

Endocrine mechanisms of puberty in heifers. Role of hypothalamo-pituitary estradiol receptors in the negative feedback of estradiol on luteinizing hormone secretion.

The hypothesis tested was that the decline in negative feedback of estradiol on secretion of luteinizing hormone (LH) that occurs as puberty approaches in heifers results from a decline in the number of receptors for estradiol in the hypothalamus and/or pituitary. In addition, associated changes in receptors for luteinizing hormone-releasing hormone (LHRH) in the pituitary, ovarian follicle development, and uterine growth were characterized. Fifty prepubertal heifers, 234 to 264 days of age, were used. Six heifers of median body weight were designated controls, and sequential blood samples were collected at 20-min intervals for 24 h every 2 wk from 249 days of age through puberty and analyzed for concentrations of LH. Frequency of LH pulses/24 h was regressed on number of days prepuberty to develop a prediction equation for puberty. Thirty of the remaining 44 heifers were killed at 253, 302, and 351 days of age (n = 10/group), and tissues for described analyses were collected. Three to 5 days before tissue collection, sequential blood samples were obtained from these heifers, as described for control heifers to determine frequency of release of LH. With this information, number of days prepuberty at the time of tissue collection was estimated from the prediction equation developed with data from control heifers. The average age at puberty in control heifers was 366 days. The average age at puberty of heifers that were not killed or included in the control group (n = 14) was 360 days. Receptor and morphological data were related to the estimated onset of puberty. Cytosolic concentration of receptors for estradiol (fmoles receptor/mg cytosolic protein) in the anterior hypothalamus, medial basal hypothalamus, and anterior pituitary declined (p less than 0.05) as puberty approached. No change in concentration of receptors for estradiol was observed in the stalk median eminence or preoptic area. The concentration of receptors for LHRH in the anterior pituitary did not change as puberty approached. Uterine weight increased rapidly during the 50 days preceding puberty. The number of small, medium, or large follicles and the wet, pressed, or dry weight of the ovaries did not change as puberty approached. Follicles with a diameter greater than 12 mm were found only in the 3 heifers estimated to be closest to puberty at the time of tissue collection. The hypothesis that the decline in estradiol feedback on secretion of LH during the prepubertal period in heifers may result from a decline in the concentration of binding sites for estradiol at the hypothalamus and/or pituitary is supported by this study.

Animals↗

PubMed1984

Relative fatty acid composition of lecithin during postmenopausal replacement therapy--a comparison between ethinyl estradiol and estradiol valerate.

The relative fatty acid composition of serum lecithin was followed in groups of women during postmenopausal replacement therapy. The effects of estradiol valerate and ethinyl estradiol in two different doses, and the modulating influence of various progestogens and antiestrogens were compared. Unopposed estrogen treatment enhanced liver lecithin synthesis along pathway I, i.e. reduced the amount of stearic acid and increased the amount of palmitic acid. The effect was clearly dose-dependent and even the low dose of 10 micrograms of ethinyl estradiol was more potent than 2 mg of estradiol valerate. No qualitative difference between the two estrogens was recorded. The sequential addition of the antiestrogen tamoxifen significantly reduced the influence of ethinyl estradiol. Liver lecithin synthesis along pathway I may be stimulated by all estrogens and not only by 17C-alkylated compounds. The prostaglandin precursors, dihomogammalinolenic and arachidonic acid, showed a seemingly dose-dependent increase during estrogen treatment. The comparatively weaker effects of estradiol valerate on lipid metabolism should make this non-alkylated estrogen the first choice in clinical practice.

Adult↗

PubMed1992

Estradiol-promoted accumulation of receptor in nuclei of porcine endometrium cells. Immunogold electron microscopy of resting and estradiol-stimulated cells.

Endometrium was collected by curettage from castrated pigs, either untreated or exposed to estradiol in vivo by intrauterine injection, and processed for electron microscopy. The resin LR Gold was used for embedding, and sections were floated on droplets of 10 nm diameter gold particles, coated with the immunoglobulin-G1 (IgG1) fraction or its Fab2 fragment of a monospecific polyclonal antiserum raised in goats against the C-terminal half of the estradiol receptor. On average, only one gold particle per microns 2 became attached in the cytoplasmic area of untreated cells, whereas four were found over the nuclear area. These figures rose to 2-3/microns 2 and 15-26/microns 2, respectively, within 10 min after exposure to estradiol. The labeling intensities of nuclei in cell clusters and of coprocessed nuclei released from cells ruptured during curettage were identical in all situations. Nuclear pores were frequently tagged after estradiol treatment. The proportions of tagging densities in nuclei of untreated and estradiol-exposed cells corresponded to those of receptor contents measured in extracts of isolated nuclei by ligand binding. This correlation was not seen for the cytoplasmic compartment of untreated cells, the scarce tagging of which is interpreted by hidden antigenic determinants. Our morphological analyses support the conclusions drawn from biochemical data (Sierralta et al., 1992) of an estradiol-promoted translocation of receptor from the cytoplasm into the nucleus.

Animals↗

PubMed1975

Effects of two estradiol antagonists upon the estradiol uptake in the rat brain and peripheral tissues.

Two estradiol antagonists, Parke-Davis CI 628 and CI 680, were studied for their inhibitory potency against labeled estradiol uptake within the hypothalamus, cerebral cortex, pituitary and uterus of the ovariectomized rat. Both drugs, tested from 15 min to 24 h prior to estradiol, induced a fast and long-lasting decrease of the hormone uptake. Three degrees of inhibition were observed depending on the tissue studied: (a) the most important inhibition concerned uterus and pituitary, where the estradiol uptake was prevented by up to 90% by the largest doses of antagonists used (6.3 and 6.1 mg, respectively, for CI 268 and CI 680); (b) in the hypothalamus, the estradiol uptake was counteracted to a lower degree; the inhibition being 39% for anterior hypothalamus and 22% for medial posterior hypothalamus; (c) cerebral cortex uptake was completely unaffected by pretreatments with the antagonists. After subcellular fractionation it was observed that the nuclear uptake of estradiol was completely abolished in both hypophyseal and hypothalamic tissues if the hormonal injection was preceded by the administration of 6.3 mg of CI 628.

Animals↗

PubMed1984

Evidence that somatostatin (SRIF14) is the primary coligand in pancreas required for specific binding of [3H]estradiol in pancreatic tissue: demonstration that [3H]estradiol and [125I]SRIF14 form complexes of varying size with a specific binding protein.

There is present in rat pancreas a protein that requires an accessory factor in order to bind [3H]estradiol. To identify this accessory factor 874g of dog pancreas were acid extracted, and following selective filtration and dialysis, the low molecular weight constituents (less than 10,000) were concentrated by lyophilization. Samples of this lyophilizate were fractionated by high performance liquid chromatography (HPLC) and eluate fractions analyzed for their capacity to enhance binding of [3H]estradiol to a protein fraction from rat pancreas that had been purified relatively free of endogenous accessory factor. Such enhancement of [3H]estradiol-binding activity eluted predominantly in one peak that coincided with the elution profile of pure somatostatin (SRIF14). Analysis of eluate fractions for somatostatin-like immunoreactive material (SLIM) indicated coincidence of SLIM with the factor that enhanced binding of [3H]estradiol. It appears likely that accessory factor in pancreas is primarily somatostatin (SRIF14). Following incubation of [125I]SRIF14 and [3H]estradiol with a partially purified binding-protein fraction from rat pancreas, a complex containing labeled [125I] and [3H] was separated by Sephadex G-200 column chromatography. In the presence of 25 microM SRIF14, which activates [3H]estradiol-binding maximally in the presence of 10 nM steroid, a protein peak containing both radiolabeled ligands eluted in the void volume indicating an apparent molecular size in excess of 200,000 Daltons. At a concentration of 1 microM SRIF14, a complex eluted at a position corresponding to an apparent Mr of 120,000. Evidently, the steroid and polypeptide mutually enhance binding to this pancreatic protein, and depending on their concentrations form structures of widely varying sizes.

Animals↗

PubMed1990

Estradiol increases phosphorylation of the 90 kDa heat shock protein not associated with estradiol receptor in MCF-7 cells in culture.

MCF-7 cells in monolayer culture were incubated with [32P]orthophosphate for 18 h followed by covalent whole cell labelling of the estradiol receptor with tritiated tamoxifen aziridine [( 3H]TA). The heat shock protein (hsp-90) bound to receptor was precipitated with monoclonal antibodies H222 or JS 34/32, coupled to protein A-Sepharose and purified by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) under reducing conditions. Hsp-90 not associated with receptor was similarly purified after isolation with the monoclonal antibody AC88. It was found that estradiol treatment of the cells markedly increased phosphate incorporation in the free hsp-90, without affecting heat shock protein bound to receptor. A 6-fold increase in phosphate content was observed after 10 min incubation of the cells with estradiol. A similar effect was seen after treatment of the cells with the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA). The calcium ionophore A23187 had no influence on hsp-90 phosphorylation, and treatment of the cells with forskolin to increase the cellular content of cAMP had a reverse effect. A 50% reduction of the phosphate content in the free hsp-90 was observed after 15 min treatment. The observation that estradiol, TPA and forskolin had effect only on hsp-90 not bound to receptor is an indication that the receptor-hsp-90 complex exists in vivo. Time course studies show that the effect of estradiol is non-genomic. Two possible explanations of the results seem to exist. Either estradiol induces an increase in the degree of phosphorylation of hsp-90, or hsp-90 is translocated to the cytosol from a different cellular compartment.

Blotting, Western↗

PubMed1997

Novel "scavestrogens" and their radical scavenging effects, iron-chelating, and total antioxidative activities: delta 8,9-dehydro derivatives of 17 alpha-estradiol and 17 beta-estradiol.

Antioxidant effects of delta 8,9-dehydro derivatives of 17 alpha-estradiol and 17 beta-estradiol were investigated using four different in vitro models: rat synaptosomal lipid peroxidation induced by Fenton's reagent, Fe(II)-chelating activities, the formation of superoxide anion radicals, and total antioxidative activities. The parent molecules, 17 alpha-estradiol and 17 beta-estradiol as well as estrone and estriol inhibit iron-dependent lipid peroxidation and stimulate total antioxidant activity. In contrast, delta 8,9-dehydro estrogens such as J811, J861, J835, or J851 not only exhibit the antioxidative activities as the parent molecules do but also directly alter the iron redox chemistry and drastically inhibit the formation of superoxide anion radicals generated by a xanthine/xanthine oxidase-dependent luminescence reactions. These in vitro findings indicate that 17 alpha-estradiol as well as 17 beta-estradiol, modified with an additional double bond in the basic structure, trigger more potent antioxidant properties. These results suggest that relatively minor modifications in the chemical structure of estrogenic compounds can enhance antioxidative actions.

Acridines↗

PubMed2003

Five-year changes in bone density, and their relationship to plasma estradiol and pretreatment bone density, in an older population of postmenopausal women using long-term estradiol implants.

The aim of this study was to observe whether bone mineral density (BMD) improves over 5 years in older women using estradiol implants. A total of 18 women were selected who had commenced hormone replacement therapy (HRT) around the age of 60 years. The median age was 60.9 years (range 59.7-63.2 years). Each woman had a pretreatment bone scan and then received 6-monthly subcutaneous 50 mg estradiol implants. Twelve untreated women were also selected who had had bone scans at baseline and after 5 years. A comparison of the changes in BMD between treated and untreated women was made using the Wilcoxon rank-sum test. All changes at the hip and spine were statistically significant improvements from baseline in the estradiol-treated group. After 5 years of treatment, the estradiol-treated group had significantly improved bone mineral densities compared with the untreated group. At the spine, the plasma estradiol concentration is statistically significantly correlated with the 5-year increase in bone density (r = 0.717, p = 0.004). There was found to be an inverse relationship between the percentage increase in BMD over the 5-year period and initial bone density (r = -0.635, p < 0.005). Thus estrogen is seen to have the effect of improving bone density in older women over 5 years of treatment. The increase in vertebral bone density is most marked in those women with the highest plasma estradiol levels and the lowest pretreatment bone density.

Bone Density↗

PubMedDate not supplied

Exogenous estradiol reduces inhibition of luteinizing hormone by estradiol in prepubertal heifers.

The hypothesis that high levels of exogenous estradiol administered to heifers during the prepubertal period would decrease subsequent negative feedback of estradiol on luteinizing hormone (LH) secretion was tested. Fourteen prepubertal heifers were ovariectomized on Day 0. Ovariectomized heifers received either no further treatment (OVX, n = 4), a single estradiol implant on Day 0 (OVXE, n = 5), or the single implant on Day 0 and two additional implants between Days 16 and 30 (OVXE+ E, n = 5). Ten ovary-intact heifers received either no treatment (INT, n = 5) or were administered the two estradiol implants between Days 16 and 30 (INT+ 5, n = 5). Comparison of LH secretion in OVXE to OVXE+E, and in INT to INT+E resulted in significant time-by-treatment interactions (p less than 0.05 for both). As pubertal age approached, mean concentration of LH (p less than 0.05) and pulse frequency (p less than 0.05) increased more rapidly in OVXE+E and INT+E than in OVXE and INT, respectively. Amplitude of LH pulses was unaffected by treatment. When data were standardized to day of puberty in INT and INT+E heifers, mean LH concentration and LH pulse frequency increased as puberty approached in both groups. These data confirm earlier reports indicating that secretion of LH increases gradually as puberty approaches in heifers. It was concluded that administration of estradiol during the prepubertal period hastened the decline in the subsequent negative feedback of estradiol. Precocious puberty was not induced in ovary-intact females.

Animals↗

PubMed2001

Decline in circulating estradiol during the periovulatory period is correlated with decreases in estradiol and androgen, and in messenger RNA for p450 aromatase and p450 17alpha-hydroxylase, in bovine preovulatory follicles.

The preovulatory surge of gonadotropins induces meiotic maturation of the oocyte, the follicular/luteal phase shift in hormone production, and ovulation. This complex and rapid series of developmental changes is difficult to study in large mammals, such as primates and ruminants, because variability in the length of individual reproductive cycles makes it virtually impossible to predict the time of the LH surge. We have validated an experimental model for inducing the LH surge and ovulation in cattle and used it to study the sequence of changes in hormone secretion and some of the mechanisms of these changes. Luteolysis and a follicular phase were induced by injection of prostaglandin F(2alpha); injection of a GnRH analogue 36 h later induced an LH surge and ovulation. The LH surge peaked 2 h after GnRH and ovulation followed 22-31 h after the surge, consistent with the periovulatory interval in natural cycles. The ensuing luteal phase was normal, both in length and in concentrations of circulating progesterone. In experiment I, the uteroovarian effluent was collected, via cannulation of the vena cava, at frequent intervals relative to GnRH injection. Circulating estradiol declined progressively after GnRH, reaching a nadir by 8-10 h before ovulation, whereas concentrations of androstenedione and testosterone remained constant. In experiment II, preovulatory follicles were obtained at 0, 3.5, 6, 12, 18, or 24 h after GNRH: Concentrations of androgens and estradiol were measured in follicular fluid and medium from cultures of follicle wall (theca + granulosa cells); steady-state levels of mRNA for 17alpha-hydroxylase (17alphaOH) and P450 aromatase were measured in follicular tissue. Shortly after the LH surge (3.5 h post-GnRH) there was an acute increase in the capacity of follicular tissue to secrete androstenedione, but not estradiol, in vitro. Thereafter, both androgens and estradiol declined, both in follicular fluid and in medium collected from cultures of follicle wall. Levels of mRNA for 17alphaOH and aromatase in follicle wall decreased significantly by 6 h after GnRH, suggesting that declining levels of these enzymes underlie the decreases in steroid production by follicular cells. These results show that in cattle the preovulatory decrease in follicular estradiol production is mediated by redundant mechanisms, because androgen production and the capacity of granulosa cells to convert androgens to estradiol decline coordinately, in concert with decreases in mRNA for 17alphaOH and P450 aromatase.

Androgens↗

PubMed1979

Serum levels of estrone and estradiol after implantation of estradiol pellets.

Serum estrone, estradiol, progesterone, FSH, and LH levels were studied after the implantation of estradiol pellets in female volunteers in the reproductive age group. The estradiol pellets were implanted at six-month intervals. The first implant consisted of four pellets (25 mg each). Subsequent implants consisted of a reduction by one pellet as compared to the previous implant. The mean serum estradiol levels during the six-month period of implantation or at the end of six-month intervals were in the premenopausal range and did not differ significantly during the study. The serum estrone levels showed a tendency to increase with time even though the number of pellets implanted was decreasing, apparently a result of incomplete absorption of the implanted estradiol during the six-month period. The results of serum progesterone determinations and basal body temperature records indicate that the suppression of ovulation takes place most consistently during the second and subsequent months after estradiol pellet implantation.

Adolescent↗