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PubMed1994

8-Hydroxylation of guanine bases in kidney and liver DNA of hamsters treated with estradiol: role of free radicals in estrogen-induced carcinogenesis.

The chronic administration of estradiol induces a high incidence (80-100%) of renal tumors in male Syrian hamsters. As part of our examination of a mechanism of carcinogenesis by free radicals generated during redox cycling of catecholestrogen metabolites, we assayed levels of 8-hydroxy-2'-deoxyguanosine (8-OHdGua), a marker product of hydroxy radical interaction with DNA, in livers and kidneys of hamsters treated with estradiol. Injections of 50 and 100 mg/kg estradiol doubled renal 8-OHdGua levels over controls [10.0 +/- 0.1 (SD) and 5.4 +/- 0.4 8-OHdGua/10(5) dGua, respectively] and raised hepatic 8-OHdGua levels almost 4-fold over control values, respectively. These changes were observed in kidney 4 h and in liver 1 or 2 h after treatment of hamsters with estradiol. Estradiol implants administered to hamsters for 3 days raised renal levels of 8-OHdGua by 50% over control values. Six days after 17 beta-estradiol implantation, 8-OHdGua levels returned to near-normal values. Liver DNA was not affected by estradiol implants. These data support a mechanism of estrogen-induced carcinogenesis by free radicals generated via redox cycling of catecholestrogen metabolites.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1993

Estradiol attenuates alpha 2-adrenoceptor-mediated inhibition of hypothalamic norepinephrine release.

These studies tested the hypothesis that estradiol facilitates norepinephrine (NE) neurotransmission by modulating alpha 2-adrenoceptor-mediated inhibition of NE release. KCl-induced overflow of 3H from superfused slices preloaded with 3H-NE was Ca2+ dependent. Hypothalamic slices from estradiol-treated rats exposed to a single KCl pulse (S1) had modestly (20%) but significantly elevated NE release when compared to slices from ovariectomized (OVX) rats. Blockade of alpha 2-adrenoceptors by pretreatment with the imidazoline antagonists idazoxan (IDA) and RX821002 (RX) markedly facilitated NE release during S1 in hypothalamic slices from OVX rats; this facilitation was attenuated or absent in slices from estradiol-treated rats. In additional studies slices were stimulated twice, 24 min apart (S1 and S2), for 3 min with 20 mM KCl. In the absence of drug, the amount of 3H-NE released during S2 was always less than the amount released during S1 (i.e., S2:S1 approximately 0.6), regardless of whether slices were from OVX or estradiol-treated females. When 10 microM IDA was applied after S1 and 15 min prior to S2, the S2: S1 ratio increased to 1.8 +/- 0.1 in hypothalamic slices from OVX animals. In contrast, the S2:S1 ratio rose only to 1.1 +/- 0.2 in slices from estradiol-treated animals. RX applied before S2 markedly increased the S2:S1 ratio in both hypothalamic and preoptic area slices from OVX rats but failed to increase the S2:S1 ratio in slices from estradiol-treated rats. Interestingly, the modest effects of alkaloid alpha 2-antagonists such as yohimbine and rauwolscine on NE release in hypothalamic and preoptic area slices were not modified by estradiol.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1976

[Cytosolic and nuclear estradiol receptors in the fetal guinea pig uterus].

After administration in situ of 3H-estradiol (8 X 10(-10) moles) to Guinea Pig fetuses (48-58 days of gestation) the presence of specific estradiol receptors in the cytosol and in the nuclear extracts of the fetal uterus has been demonstrated. The presence of these estradiol receptors was confirmed after incubation of the same fetal tissues with 3H-estradiol (8 X 10(-8) M). Estradiol has a significant competitive effect on the 3H-estradiol-complex; estrone and estriol also have an effect but less intense. Testosterone, cortisol, aldosterone have no effect. By ultracentrifugation in sucrose density gradient of the cytosol fraction a component with a sedimentation coefficient of 8.5-9 S is observed. The dissociation constant of the 3H-estradiol receptor has a high affinity (KD = 4 X 10(-10) M).

Aldosterone↗
PubMed1993

[Estradiol-binding properties of a sheep haptoglobin complex with hemoglobin. II. Preliminary data on quantitative characteristics of interaction].

The estradiol-binding properties of the sheep haptoglobin-hemoglobin complex (Hp-Hb) have been studied. The time and temperature dependencies of the steroid binding have been established the tightly bound 17 beta-estradiol, which is not detached from the complex during precipitation or extraction, has been shown to form a part of the total amount of the steroid capable of bending to Hp-Hb. Disturbances in the protein-protein interactions between Hp and Hb lead to the dissociation of estradiol as well as to the loss by the protein of its estradiol-binding activity. The values of relative competitive activity for several steroids suggest that some structural elements of the 17 beta-estradiol molecule play a role in estradiol-protein interactions. It is assumed that the Hp-Hb complex has two or more 17 beta-estradiol binding sites.

Animals↗
PubMed1996

17 beta-estradiol inhibits proliferation and migration of human vascular smooth muscle cells: similar effects in cells from postmenopausal females and in males.

OBJECTIVES: Cardiovascular disease is rare in premenopausal women, but increases after the menopause when hormone replacement therapy reduces coronary events. Vascular smooth muscle cell (SMC) proliferation and migration occur in atherosclerosis, restenosis and venous graft disease. We studied the effects of 17 beta-estradiol on SMC proliferation and migration. METHODS: SMC were cultured from saphenous veins of postmenopausal women and age-matched men. Cell growth was determined by 3H-thymidine incorporation and cell counting. Migration of SMC was assessed in 4-well chambers. SMC were seeded in one corner and PDGF-BB in filter paper glued onto the opposite wall. RESULTS: PDGF-BB (5 ng/ml for 24 h) similarly stimulated 3H-thymidine incorporation in female (511 +/- 57%; n = 8) and male (528 +/- 62%; n = 12) SMC. This was reduced by 17 beta-estradiol (10(-8)-10(-6) M; female 313 +/- 52%; male 337 +/- 54%; P < 0.05). PDGF-BB increased the number of SMC (P < 0.0001 at 10 days) obtained from females (153 +/- 3%; n = 5) and males (150 +/- 4%; n = 5), which was inhibited by 17 beta-estradiol (10(-6) M; female 134 +/- 7%; male 128 +/- 5%; P < 0.05). Similar results were obtained with basic fibroblast growth factor. In contrast to 17 beta-estradiol, another steroid (dexamethasone) had no effects on 3H-thymidine incorporation in these cells stimulated with PDGF-BB, PDGF-BB (0.01-1 ng) stimulated SMC migration (P < 0.05) which was inhibited by 17 beta-estradiol (10(-10)-10(-6) M; n = 5; P < 0.005). CONCLUSION: 17 beta-Estradiol inhibits growth-factor-induced SMC proliferation and migration regardless of gender. These effects of 17 beta-estradiol may contribute to its cardiovascular protective properties in postmenopausal women during replacement therapy.

Aged↗
PubMed1997

Estradiol increases the sensitivity of hippocampal CA1 pyramidal cells to NMDA receptor-mediated synaptic input: correlation with dendritic spine density.

Previous studies have shown that estradiol induces new dendritic spines and synapses on hippocampal CA1 pyramidal cells. We have assessed the consequences of estradiol-induced dendritic spines on CA1 pyramidal cell intrinsic and synaptic electrophysiological properties. Hippocampal slices were prepared from ovariectomized rats treated with either estradiol or oil vehicle. CA1 pyramidal cells were recorded and injected with biocytin to visualize spines. The association of dendritic spine density and electrophysiological parameters for each cell was then tested using linear regression analysis. We found a negative relationship between spine density and input resistance; however, no other intrinsic property measured was significantly associated with dendritic spine density. Glutamate receptor autoradiography demonstrated an estradiol-induced increase in binding to NMDA, but not AMPA, receptors. We then used input/output (I/O) curves (EPSP slope vs stimulus intensity) to determine whether the sensitivity of CA1 pyramidal cells to synaptic input is correlated with dendritic spine density. Consistent with the lack of an estradiol effect on AMPA receptor binding, we observed no relationship between the slope of an I/O curve generated under standard recording conditions, in which the AMPA receptor dominates the EPSP, and spine density. However, recording the pharmacologically isolated NMDA receptor-mediated component of the EPSP revealed a significant correlation between I/O slope and spine density. These results indicate that, in parallel with estradiol-induced increases in spine/synapse density and NMDA receptor binding, estradiol treatment increases sensitivity of CA1 pyramidal cells to NMDA receptor-mediated synaptic input; further, sensitivity to NMDA receptor-mediated synaptic input is well correlated with dendritic spine density.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMedDate not supplied

Influence of estradiol and androstenedione on ACTH and cortisol secretion in the ovine fetus.

OBJECTIVE: To test the hypothesis that physiologic increases in fetal plasma 17 beta-estradiol and androstenedione modulate the activity of the fetal hypothalamic-pituitary-adrenal (HPA) axis. METHODS: Seventeen pregnant ewes and their fetuses were chronically catheterized. At the time of surgery, the fetuses received implants that released 17 beta-estradiol (n = 5) alone or 17 beta-estradiol and androstenedione (n = 6), each at a rate of approximately 250 micrograms/day for each steroid. The control group (n = 6) received either no pellet (n = 2) or a "placebo" pellet, which contained no steroid (n = 4). Fetal blood samples were drawn for hormone and blood gas analysis at 1-3-day intervals until the time of spontaneous parturition. Fetal plasma ACTH and cortisol concentrations were fit to semilogarithmic equations and analyzed by stepwise multiple linear regression analysis for statistically significant effects of 17 beta-estradiol and androstenedione. RESULTS: Estradiol significantly increased and androstenedione significantly decreased the ACTH and cortisol concentrations. Treatment with both 17 beta-estradiol and androstenedione resulted in parturition approximately 4 days earlier than in the other groups (P < .05). CONCLUSIONS: Physiologic increases in fetal plasma estradiol and androstenedione modify the activity of the HPA axis.

Adrenocorticotropic Hormone↗
PubMed1998

A comparison of three preinduction cervical priming methods: prostaglandin E2 gel, Dilapan S rods and Estradiol gel.

The aim of the study was to evaluate the efficacy of three cervical priming methods. From January 1, 1994 to December 31, 1996 247 patients presenting an indication for induction of labor with an unripe cervix were randomly assigned to one of the following preinduction protocols: 0.5 mg of Prostaglandin E2 gel administered intracervically (n = 83), four hygroscopic Dilapan S rods applied intracervically (n = 82), and 150 mg of Estradiol gel administered intravaginally (n = 82). The inclusion criteria were the patient's informed consent, singleton pregnancy of more than 36 weeks, cephalic presentation, Bishop score < 5 points and reactive non-stress test. If the cervical maturation (Bishop score > or = 5, and/or Bishop score augmentation by 2 points) did not occur after 14 hours of priming, the case was considered a failure. In the opposite case the patient was induced by means of extraamniotic PGE2 administration. The mean gain in the Bishop score was 3.7 points in the PGE2 group 3.9 points in the Dilapan S group, and 2.8 points in the Estradiol group. 71 patients (85.5%) were successfully preinduced in the PGE2 group, 73 (89.0%) in the Dilapan S group, and 63 (76.8%) in the Estradiol group. Labor was induced by preinduction only in 23 patients (31.3%) of the PGE2 group in 17 (20.7%) of the Dilapan S group, and in 14 (17.1%) of the Estradiol group. The mean induction to delivery interval was 7 h 27 min in PGE2 group, 7 h 49 min in the Dilapan S group and 9 h 15 min in the Estradiol group. The Caesarean section rate was 24.4% in the PGE2 group, 10.5% in the Dilapan S group, and 24.4% in the Estradiol group. PGE2 gel and Dilapan S rods proved higher efficacy than Estradiol gel. The highest frequency of labor induced by preinduction only was in the PGE2 group. There were shorter induction to delivery intervals in the PGE2, and Dilapan S groups. The lowest Caesarean section rate was in the Dilapan S group. Neither serious side effects nor negative neonatal outcome were noted in either group.

Adult↗
PubMed1998

Estradiol as an antioxidant: incompatible with its physiological concentrations and function.

Estradiol has been documented to inhibit the oxidation of low density lipoprotein (LDL). We show that physiological concentrations of estradiol do not inhibit the oxidation of LDL by copper. LDL samples isolated from a) premenopausal and postmenopausal women and from b) women at different time periods during their menstrual cycle, who differ vastly in plasma estradiol levels, were also oxidized at the same rates by copper. In contrast, LDL samples isolated from c) women who were hyperstimulated during in vitro fertilization (IVF), with estradiol concentrations above 2000 pg/ml, were resistant to oxidation by copper. However, these LDL samples were also oxidized at a higher rate by peroxidases. More importantly, subjects with high estradiol levels also showed an increase in myeloperoxidase (MPO) protein in the plasma. Based on these results, we conclude that at physiologic concentrations, it is unlikely that estradiol could act as an antioxidant. In fact, the ability of estradiol to induce MPO and become a prooxidant might instead suggest that MPO-mediated oxidative clearance of LDL from plasma by liver might favorably influence the outcome of atherosclerosis.

Adult↗
PubMed1998

Induction of progestin receptors by estradiol in the forebrain of estrogen receptor-alpha gene-disrupted mice.

Mice, rats, and humans have two types of estrogen receptors, estrogen receptor-alpha (ERalpha) and estrogen receptor-beta (ERbeta). Estrogen receptor-alpha gene-disrupted (ERalpha-disrupted) mice bear two nonfunctional copies of the ERalpha gene. This mutation blocks the synthesis of full-length ERalpha, renders the animals infertile, and inhibits the induction of female sexual behaviors by estradiol and progesterone. It is likely that many of the processes contributing to the regulation of sexual receptivity by estradiol and progesterone are compromised in ERalpha-disrupted mice. However, given the importance of progesterone in the regulation of sexual receptivity and given the importance of progestin receptors (PRs) in mediating the responses of females to progesterone, we investigated the effects of ERalpha disruption on the induction of PRs by estradiol in the forebrain. We hypothesized that estradiol would induce PRs in wild-type mice but not in ERalpha-disrupted mice. Ovariectomized wild-type and ERalpha-disrupted mice were implanted with either estradiol-filled capsules or empty capsules for 5 d, after which their brains were processed for the immunocytochemical detection of PR. Estradiol increased the number of PR-immunoreactive cells in both wild-type and ERalpha-disrupted mice. The residual responsiveness of ERalpha-disrupted mice to estradiol could be accounted for by an ERbeta-dependent mechanism or another as yet unidentified estrogen receptor; however, because ERalpha-immunoreactivity and PCR product representing the 3' end of ERalpha mRNA were found in at least one PR-containing region of the ERalpha-disrupted mice, an ERalpha splice variant may also mediate the induction of PR-immunoreactivity in ERalpha-disrupted mice.

Animals↗
PubMed1980

Pharmacokinetic studies on low dose estradiol 17 beta administered orally to postmenopausal women.

Peripheral plasma from four postmenopausal women was analysed for estrone, estradiol, lutenizing hormone and follicle stimulating hormone during 24 hours following an oral intake of a single dose of 1.0 mg micronized estradiol, on the first day of therapy and after one month. A similar study was carried out with another four postmenopausal patients, who received 0.2 mg estradiol three times daily. The measurements were performed by radioimmunoassay (RIA). It is concluded that the plasma concentrations of estrone and estradiol are higher and those of FSH lower after one month of therapy than on the first treatment day, while plasma LH remains unchanged. Micronized estradiol is rapidly absorbed from the gastrointestinal tract and converted to estrone, and the plasma profiles of estrone during the day are more constant with a divided daily dose than with a single higher dose. The divided daily dose results in an equally good clinical effect even though the total administration of estradiol is lower.

Administration, Oral↗
PubMed1992

Regulation of estrus and ovulation in mares with progesterone or progesterone and estradiol biodegradable microspheres with or without PGF2alpha.

A single injection of a microsphere preparation, designed to deliver 1.25 gm progesterone and 100 mg estradiol-17beta at a controlled rate, for a duration of 12 to 14 days, produces accurate control of estrus and fertile ovulations in mares. Treatment is followed by PGF2alpha injection 14 days after steroid injection. The objectives of the present study were to determine whether estradiol added to the progesterone treatment or PGF2alpha administered at the end of the steroid treatment regimen, would improve synchronization of estrus and ovulation. A total of 45 cyclic horse mares was randomly assigned to 1 of 5 treatment groups as follows: Group 1 (control, n=9) sterile microsphere vehicle+sterile PGF2alpha vehicle 14 days after treatment with microsphere vehicle; Group 2 (n=9) progesterone and estradiol microspheres+PGF2alpha 14 days after treatment with microspheres; Group 3 (n=9) progesterone and estradiol microspheres+PGF2alpha vehicle 14 days after treatment with microspheres; Group 4 (n=9) progesterone + PGF2alpha 14 days after treatment with microspheres; and Group 5 (n=9) progesterone+PGF2alpha vehicle 14 days after treatment with microspheres. Addition of estradiol (P<0.05) or PGF2alpha (P<0.05) to the treatment regimen increased synchronization efficary by reducing variation in days to ovulation. All treatments significantly reduced variation in days to estrus compared with that of the controls; however, mares in the progesterone groups had an increased incidence of silent or shortened estrous behavior ( 2 days in duration compared with mares treated with progesterone (78 vs 33%, respectively). Therefore, estradiol and PGF2alpha each appear to reduce variation in days to ovulation while estradiol seems to promote better expression of posttreatment estrous behavior.

Journal Article↗
PubMed1996

Alterations in follicular estradiol and gonadotropin receptors during development of bovine antral follicles.

It was hypothesized that growth divergence of dominant and subordinate follicles during Wave 1 and growth termination of the dominant follicle would be associated with changes in the number of gonadotropin receptors on granulosa cells and estradiol in follicular fluid. To test this hypothesis, follicular development of 16 Holstein heifers was monitored by ultrasound, and follicles were collected on Days 2,4,6 and 10 (Day 0 = ovulation). Dominant follicles were compared across days, whereas dominant and largest subordinate follicles were compared on Days 2 and 4 only. The numbers of LH and FSH receptors on the granulosa cells of dominant follicles did not differ significantly over Days 2, 4, 6 and 10. In contrast, concentrations of estradiol in follicular fluid decreased (P < 0.05) from Days 2 to 10 (373 +/- 150 to 42 +/- 12 ng/ml) and concentrations of progesterone in follicular fluid increased (P < 0.05) from Days 2 to 10 (12.2 +/- 2.3 to 24.4 +/- 4.8 ng/ml). Correspondingly, the ratio of estradiol:progesterone in the dominant follicles decreased (P < 0.05) from Days 2 to 10. Comparisons between dominant and subordinate follicles indicated greater (P < 0.05) estradiol concentrations in the dominant follicle on Day 2, but the number of gonadotropin receptors was not different until Day 4. Thus, differences in concentrations of follicular fluid estradiol, but not numbers of granulosa cell gonadotropin receptors, were associated with the early growth divergence of dominant and subordinate follicles (Day 2) and the eventual growth termination of the dominant follicle (Day 10). Late divergence (Day 4) was associated with higher gonadotropin receptor numbers and follicular estradiol concentrations in the dominant than in the subordinate follicles. These results indicate that an increase in estradiol productivity of the selected dominant follicle occurred before an increase in the number of gonadotropin receptors.

Journal Article↗
PubMed1997

Ovulatory responses and plasma luteinizing hormone concentrations in dairy heifers after treatment with exogenous progesterone and estradiol benzoate.

The objectives of this experiment were to determine the effects of 0.5 mg estradiol benzoate, administered intramuscularly 24 h after removal of CIDR-B progesterone containing intravaginal devices, on the time to estrus, ovulation and peak LH concentration in dairy heifers. Ovulatory responses and plasma LH concentrations were examined using 14 Friesian dairy heifers in 2 separate treatment periods. All heifers received a CIDR-B progesterone-containing intravaginal device with an attached 10-mg estradiol benzoate capsule for 12 d. Within each period, 24 h after CIDR-B removal, 7 heifers received an intramuscular injection of 0.5 mg estradiol benzoate while the remaining 7 heifers received an intramuscular injection of a placebo. Blood samples for LH assay were collected at 0, 6 and 12 h, and then every 4 h for 60 h after estradiol injection. Detection of estrus was conducted at 4-h intervals, and ultrasonographical examination to detect ovulation was conducted every 8 h for 88 h after removal of the CIDR-B device. Treatment with estradiol benzoate tended to reduce the time from device removal to the LH peak in Period 1 (median time to LH peak 40.1 vs 63.9 h; P = 6.07). In Period 2, treatment with estradiol had no significant effect on the time to the LH peak, standing estrus or ovulation. We hypothesize that the period effect was due to the stage of cycle at the time of treatment. For heifers treated in Period 1, the stage of cycle was random. However, because of the prior synchronization of estrus, which was implicit in the experimental design, heifers in Period 2 tended to be in late diestrus. The administration of estradiol benzoate after treatment with exogenous progesterone appears to overcome the variability in timing of LH peaks typically occurring in a herd of synchronized heifers due to different stages of follicular development.

Journal Article↗
PubMed1986

Estradiol receptor: phosphorylation on tyrosine in uterus and interaction with anti-phosphotyrosine antibody.

Estradiol receptor from rat uteri incubated with [32P] orthophosphate has been purified by diethylstilbestrol--Sepharose followed by heparin--Sepharose chromatography. The purified receptor, analyzed by centrifugation through sucrose gradients after incubation with monoclonal antibodies against purified estradiol receptor, appears to be labeled with 32P. The receptor preparation has been further purified by immunoaffinity chromatography and submitted to SDS--poly-acrylamide gel electrophoresis. A heavily 32P-labeled 68 kd protein and a very lightly 32P-labeled 48 kd protein, probably a proteolytic product of the 68 kd protein, were detected. Phosphoamino acid analysis of the receptor eluted from the immunoaffinity column shows that its 32P-labeling occurs exclusively on tyrosine. This is the first report on phosphorylation on tyrosine of a steroid receptor in tissue. It is consistent with our previous finding that a uterus estradiol receptor-kinase, which confers hormone binding ability to the estradiol receptor, in vitro phosphorylates this receptor exclusively on tyrosine. Calf uterus receptor binds with high specificity and affinity to monoclonal anti-phosphotyrosine antibodies covalently bound to Sepharose (Kd = 0.28 nM). Dephosphorylation of the receptor by nuclei containing the calf uterus nuclear phosphatase abolishes the interaction with antibodies. These results suggest that also in calf uterus, estradiol receptor is phosphorylated on tyrosine. Anti-phosphotyrosine antibodies bound to Sepharose have been used to partially purify the estradiol receptor from calf uterus.

Animals↗
PubMed1995

Properties and regulation of 17 beta-hydroxysteroid oxidoreductase of OVCAR-3, CAOV-3, and A431 cells: effects of epidermal growth factor, estradiol, and progesterone.

Although there is a growing body of evidence that 17 beta-hydroxysteroid oxidoreductase plays a role in the regulation of steroid levels in epithelial tumors of the endometrium and breast, our knowledge of its role in other gynecologic tumors is limited. In this investigation, the 17 beta-hydroxysteroid oxidoreductase activity of cell lines derived from two ovarian tumors (OVCAR-3, CAOV-3) and an epidermoid tumor of the vulva (A431) was assayed under conditions which differentiate between 17 beta-hydroxysteroid oxidoreductase type 1, a cytosolic isoform highly specific for estradiol, and type 2, a membrane bound isoform reactive with both estradiol and testosterone. On the basis of estradiol/testosterone activity ratios, all three cell lines appear to have type 2-like activity, with the specific activity of A431 markedly greater than that of the other cell lines. Estradiol, progesterone, or EGF, alone or in combination, were without effect on the enzymatic activity of OVCAR-3 cells. EGF decreased the activity of CAOV-3 cells slightly. In contrast, EGF stimulated A431 17 beta-hydroxysteroid oxidoreductase activity 7-8-fold over a 5-day exposure. Estradiol or progesterone, singly or in combination, also did not effect the enzymatic activity of A431 cells. However, progesterone inhibited the increase in activity seen in the presence of EGF. With EGF, estradiol, and progesterone together, the increase in enzymatic activity was comparable to that with EGF alone. The effects of estradiol and progesterone appear to result from steroid actions following binding of EGF to low-affinity receptors on A431 cells.

Epidermal Growth Factor↗
PubMed1981

Estradiol and progesterone receptors in estrogen-primed endometrium.

Estradiol and progesterone receptor levels were measured in endometrial samples obtained from patients who were on different dosages of estradiol therapy and from women in the late proliferative phase of a normal menstrual cycle. Samples of blood were collected at the time of biopsy, and the levels of estradiol, estrone, progesterone, follicle stimulating hormone, and luteinizing hormone were measured in the serum. The patients were divided into five groups. The first group (controls) consisted of patients in their late proliferative phase. The patients in groups two, three, and five were receiving estradiol in various doses by pellet therapy, along with a cyclic progestogen each month. The women in the fourth group also had implantation of estradiol pellets but failed to take the progestogen as advised. In our series, the levels of cytoplasmic estradiol and progesterone receptors were markedly elevated in the no progestogen group compared to the controls. There was no significant difference in the levels of the receptors in the groups which took the progestogen as advised.

Endometrium↗
PubMed1982

Stimulation of 12-lipoxygenase activity in rat platelets by 17 beta-estradiol.

The effects of estradiol on the endogenous fatty acid (specifically, arachidonic acid) composition of cellular phospholipid fractions and the 12-lipoxygenase activity in rat platelets in vivo were studied. Estradiol had no significant effect on the endogenous fatty acid composition of cellular phospholipid fractions. However, estradiol significantly increased 12-lipoxygenase activity in platelets in a dose-dependent manner. The stimulatory effect of estradiol on platelet lipoxygenase was blocked by the anti-estrogen nafoxidine hydrochloride which was injected simultaneously together with estradiol in vivo, suggesting that the effect in target cells was due directly to estradiol.

Animals↗