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PubMed1985

Estradiol-induced increase of specific [3H]ketanserin binding sites on rat uterine membranes.

[3H]Ketanserin, a specific serotonin (5-HT) antagonist, was used to investigate whether 5-HT receptors increased in the uterine membranes of ovariectomized rats on administration of 17 beta-estradiol-3-benzoate (estradiol) and also to investigate the characteristics of specific [3H]ketanserin binding to the uterine membranes from estradiol-treated ovariectomized rat. Administration of estradiol significantly increased the amount of [3H]ketanserin specifically bound at equilibrium but did not change the apparent affinity of specific [3H]ketanserin binding. The specific [3H]ketanserin binding to estradiol-treated ovariectomized preparations was rapid and reversible. The Scatchard plots of the saturation curves of specific [3H]ketanserin binding to untreated and estradiol-treated ovariectomized preparations were convex. The apparent Ki values of various serotonergic agents deduced from displacements by these compounds of specific [3H]ketanserin binding to estradiol-treated ovariectomized preparations were two to four orders of magnitude smaller than those of adrenergic, dopaminergic and histaminergic agents. These results suggest that [3H]ketanserin binds mainly to 5-HT receptors in the uterine membranes of estradiol-treated ovariectomized rats.

Animals↗
PubMed1994

Endothelium-independent relaxation by 17-alpha-estradiol of pig coronary arteries.

We have studied the effects of 17-alpha-estradiol, a non-estrogenic steroid, on pig coronary arteries contracted by K+, Ca2+ or serotonin. Experiments were performed on helicoidal strips and rings of left circumflex coronary arteries from freshly slaughtered white pigs and on helicoidal strips of rat thoracic aorta. The strips and rings were suspended inside a water-jacketed muscle chamber in an oxygenated Krebs solution at 37 degrees C. From the initial K(+)-evoked contraction, 17-alpha-estradiol caused a relaxation with an IC50 (15 microM) which was in the range of the IC50s obtained for nitroglycerin (1.3 microM) and nicorandil (50 microM). Contractions evoked by Ca2+ were inhibited by 17-alpha-estradiol, but full blockade could not be achieved. Serotonin-evoked contractions were also blocked by 17-alpha-estradiol with an IC50 of 2.1 microM; 17-beta-estradiol also inhibited the serotonin-evoked contractions. In the presence of 100 microM of the nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester, the relaxing properties of 17-alpha-estradiol in pig coronary arteries and rat thoracic aorta were unaffected, suggesting that endothelial NO release was unrelated to these effects. 17-alpha-Estradiol also relaxed denuded pig coronary artery strips, suggesting that other endothelial-derived relaxing factors were not involved in its vascular effects. The results are compatible with the idea that 17-alpha-estradiol causes relaxation of coronary vessels by acting directly on the cell membrane of smooth muscle cells; these effects seem to be unrelated to the genomic physiological effects of estrogens.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Epithelial cell involvement in the estradiol-stimulated accumulation of IgA in the rat uterus.

Immunoglobulin A (IgA) and G (IgG) were analyzed in rat plasma, uterus and uterine secretions by radioimmunoassay and in tissues by immunofluorescent microscopy to determine the mechanism by which estradiol controls IgA and IgG movement from the uterus into the uterine lumen. To determine whether there was evidence for immunoglobulin transport, plasma, tissue and uterine fluid concentrations of IgA and IgG were measured in ovariectomized rats at a time when uterine fluid IgA and IgG were elevated by treatment with estradiol. The concentration of IgA in uterine fluid was 22 times greater than that in tissue indicating that, in response to estradiol, IgA accumulated in the lumen against an apparent concentration gradient. In contrast to IgA, the concentration of IgG in uterine fluid was significantly lower than that in the uterus and in plasma. Immunofluorescent analyses indicated that estradiol has a marked effect on IgA associated with uterine epithelial cells. In saline-injected controls, small amounts of IgA were found in the epithelial cells and in the basement region of these cells. In response to estradiol, IgA accumulated in these cells at a time that coincided with the known increase of IgA in the uterine lumen. No IgA increase was observed when progesterone was given along with estradiol. Similar analyses for IgG, failed to demonstrate epithelial cell involvement of IgG into the uterine lumen. These experiments indicate that in response to estradiol, IgA is moved into the uterine lumen by a mechanism that is distinctly different from that which controls IgG. Since IgA movement is against an apparent concentration gradient, it suggests that estradiol acts on epithelial cells to regulate IgA transport from the uterus into the uterine lumen.

Animals↗
PubMed1983

Sulfhydryl sensitivity and [125I]-16 alpha-IODO-17 beta-estradiol binding of estrogen receptor in ovarian epithelial carcinomas.

We find that estrophilin from either the cytosolic or nuclear fractions of ovarian epithelial carcinomas (OVCA) binds irreversibly to controlled-pore glass beads (CPG). The CPG-adsorbed estrophilin releases [3H]-estradiol at 4 degrees C in the presence of 1.25 mM AgNO3; estradiol binding capacity from the nuclear fraction is restored by 10 mM dithiothreitol. The number of available estradiol binding sites in cytosol that are sensitive to AgNO3 correlate with (a) the number of estradiol-inhibitable binding sites found in the 8S region in low-salt sucrose gradients (r = 0.9) but not with (b) estradiol-inhibitable binding in the 4S region (r = 0.3) and thus, as expected, only poorly with (c) estimates of available cytoplasmic estrogen binding sites using a standard dextran-coated charcoal analysis (r = 0.7). Total estrogen binding extracted from the nuclear fraction with 0.5 M KCl and adsorbed to hydroxylapatite agreed with the sulfhydryl blocking reagent sensitive moiety (r = 0.9). Estrophilin from OVCA cytosol or nuclear fractions bound [125I]-16 alpha-iodo-estradiol indistinguishably from [3H]-estradiol. The two forms of radiolabelled-estradiol yielded equivalent data that demonstrated a shift in the estrogen binding moiety from the 8S region to the 4-5S region when 0.5 M KCl was added to gradient analyses of OVCA cytosols. From these observations we conclude that the estrophilin found in OVCA is similar to that found in normal and cancerous tissues of other female reproductive organs and that this estrophilin can bind a biologically active radiohalogenated estrogen potentially useful for imaging or treating these tumors.

Adult↗
PubMed1989

Comparative effects of 17 beta-estradiol, progestin R5020, tamoxifen and RU38486 on lactate dehydrogenase activity in MCF-7 human breast cancer cells.

The effects of 17 beta-estradiol (estradiol), synthetic progestin R5020 and their antagonists, tamoxifen (Tam) and synthetic RU38486 on lactate dehydrogenase (LDH) activity in MCF-7 human breast cancer cells during the growth period were studied. A specially developed quantitative cytochemical assay was used; LDH activity is expressed per cell, and is thus independent of the positive and negative growth effects of the hormones and antagonists. Estradiol and R5020 stimulated LDH activity after similar exposures (6-48 h) and the stimuli were concentration dependent over the range 10(-7) M to 10(-10) M. As for the antagonists, RU38486 stimulated LDH activity in much the same way as estradiol and R5020; Tam alone, on the other hand, does not stimulate LDH, but when added to estradiol, Tam inhibits estradiol mediated LDH activation. When present at half-stimulant concentration, estradiol + R5020 and estradiol + RU38486 exhibit additive effects on LDH activity. Thus LDH appears to be an interesting tool for the study of hormone and antagonist effects in MCF-7 breast cancer cells.

Breast Neoplasms↗
PubMed1989

Tamoxifen decreases the estradiol induced progesterone receptors by interfering with nuclear estrogen receptor accumulation.

The retention time of the estrogen receptor in the nucleus of target cells after antiestrogen treatment has been shown to be longer than after estradiol. This paper describes the accumulation of nuclear estrogen receptors and the obtention of estrogenic responses (i.e. synthesis of cytosolic progesterone receptors and DNA) in the rat uterus after tamoxifen treatment in the presence or absence of estradiol. One-week ovariectomized adult rats were implanted with a silicone elastomer capsule containing corn oil or 25 micrograms estradiol/capsule (0 h). 48 h after implantation rats were injected with corn oil or 2 mg tamoxifen/kg and decapitated at 72, 96 or 120 h after implantation. In parallel experiments the implants were removed just before the injections of tamoxifen or oil. Tamoxifen injected into rats implanted with oil increased both the occupied nuclear receptors and the progesterone receptors at 96 h. In rats implanted with estradiol, tamoxifen did not increase the occupied nuclear receptors and decreased the levels of progesterone receptor and DNA at 96 h. In rats whose estradiol implants were removed at 48 h tamoxifen did not change the level of occupied nuclear receptors at 72 h but it increased them abruptly at 96 and 120 h. In these rats progesterone receptors decreased at 72 h but they increased at 96 and 120 h, and DNA decreased at 120 h to a lower level than before implantation. The results suggest that when estradiol is acting, tamoxifen is not able to increase the level of occupied estrogen receptor and it acts as an antiestrogen by decreasing the high level of progesterone receptors previously induced by estradiol. When estradiol is not acting tamoxifen behaves as a partial estrogen agonist by inducing progesterone receptors. However, the antiestrogenic action of tamoxifen on the rat uterus DNA does not seem to be affected by estradiol.

Animals↗
PubMed1988

One day of estradiol treatment enhances platelet aggregation at the site of microvascular injury without altering aggregation ex vivo.

Mice were implanted subcutaneously with a pellet containing 0.5 mg estradiol placebo. On the day following implantation platelet aggregation was produced in arterioles on the brain surface (pial arterioles) by injuring their endothelium in vivo with a noxious light/dye stimulus. The time between the onset of the noxious stimulus and the appearance of platelet aggregates was significantly shortened (p less than .01) in the estradiol treated mice. In contrast to this enhancement of aggregation, when platelets were tested ex vivo in platelet rich plasma (PRP), aggregation to sodium arachidonate or to ADP was not altered in estradiol treated mice. Thus the enhanced aggregation observed in injured pial arterioles of estradiol treated mice may not reflect direct effects of estradiol on the platelet itself. Rather enhanced aggregation may reflect an effect of estradiol on endothelium or adjacent tissue. This effect was produced within 24 hours of achieving pregnancy levels of estradiol. The rapidity of the effect is of interest in light of earlier studies showing a similar in vivo action following 7-14 days of high estradiol levels. The rapid effect suggests that an action on megakaryocytes is an unlikely explanation for the results.

Animals↗
PubMed1984

The effect of estradiol and progesterone on the sexual behavior of ovariectomized mares.

Daily treatment (5 days) with estradiol resulted in increased levels (p less than 0.05) of proceptive behavior in ovariectomized as compared to control mares (N = 8 per treatment) within 4 hr of injection and for the 4 subsequent days. Ejaculations occurred more often (p less than 0.05) in estrogen-treated mares on days 2-5, but the number of precopulatory investigations by the stallions was not altered. Progesterone treatment resulted in an absence of sexual behavior except in one mare on Day 1. Control mares exhibited varying levels of sexual interest. The concurrent administration of estradiol and progesterone produced a biphasic effect on proximity-related behaviors. Proximity behaviors were initially (Day 1) greater and subsequently less in the group treated with both hormones than in the group treated with estradiol alone. Injections of free estradiol resulted in a shorter latency to effect for two measures of proceptivity than did injections of estradiol benzoate. A dose response test for progesterone showed no effect with 0, 1, or 10 mg, but 100 mg was inhibitory (p less than 0.05). These results demonstrated that within 4 hr estradiol stimulated, while progesterone inhibited estrous behavior in ovariectomized mares and that concurrent administration of estradiol and progesterone produced a biphasic effect, first enhancing, then suppressing some aspects of the estrous response. The relatively short latency to action of all treatments and the biphasic effect of concurrent estradiol and progesterone may be attributable to low level, endogenous hormones.

Animals↗
PubMed1991

Effects of estradiol replacement in ovariectomized rats on conditioned avoidance responses and other behaviors.

The acquisition of conditioned avoidance responses along with spontaneous behaviors were studied in ovariectomized rats. Fourteen days after ovariectomy, they were injected subcutaneously with one of the following doses of estradiol benzoate: 0.2, 2 or 20 microgram/rat. Behavioral tests were applied 3, 24, 48 or 72 hours after estradiol treatment. Although estradiol 2 microgram/rat induced a decrease in acquisition of conditioned avoidance responses at all times tested, this effect was maximum at 48 h. Estradiol 0.2, and 20 microgram/kg decreased and stimulated, respectively, the acquisition performance, as tested 3 h after injection. All doses increased global motility and rearing behavior. This hypermotility disappeared at 24 h, but it was observed again at 48 and 72 h after estradiol 0.2 and 20 microgram/rat. The hormone also induced an increase in head shaking and a decrease in grooming. Although the behavioral changes are more significant in presence of very low serum levels of estradiol, they seem to be triggered by the previous increase in the estradiol levels. The possible sites and mechanisms of action of estradiol on behavior are discussed.

Animals↗
PubMed1992

Interaction of estradiol, testosterone, and progesterone in the modulation of hormone-dependent aggression in the female rat.

Female rats that had become aggressive as a result of cohabiting with a sterile male were ovariectomized and implanted with Silastic tubes of estradiol, testosterone, and progesterone, estradiol and testosterone alone, or with empty tubes. The implants were designed to model serum concentrations present during the last week of pregnancy (estradiol, 0.06 ng/ml; testosterone, 2.6 ng/ml; progesterone, 70 ng/ml). Following a test of aggression 1 week postoperatively, estradiol and testosterone implants were replaced with ones designed to maintain the lower hormone levels present following parturition (0.02 ng/ml; 0.6 ng/ml, respectively). Progesterone was not replaced. At the first aggression test, females with estradiol and testosterone alone displayed significantly more aggression than females with these hormones plus progesterone. Both groups were more aggressive than females without hormone replacement. Following the exchange of large implants for small ones, females that previously had progesterone increased in aggression while females that previously had only estradiol and testosterone decreased in aggression. Both groups continued to be more aggressive than the group without hormone replacement. High serum progesterone present near the end of pregnancy appears to moderate the expression of aggression supported by estradiol and testosterone. Conversely, progesterone's decline at parturition appears to produce a rebound facilitation of aggression even though serum estradiol and testosterone simultaneously decline.

Aggression↗
PubMed1991

Biotransformation of estradiol by explant culture of human mammary tissue.

In vivo experiments on strains of mice that differ in the risk of developing mammary cancer have demonstrated a correlation between the extent of 16 alpha-hydroxylation of estradiol and incidence of mammary cancer. The ability of human mammary terminal duct lobular unit (TDLU), the site of neoplastic transformation, to metabolize estradiol or to accumulate estradiol metabolites has not been unequivocally established. Using a newly developed human mammary TDLU explant culture system and a radiometric assay for estradiol metabolism, we compared the site-specific metabolism of estradiol by the 17-oxidation, 2-hydroxylation, and 16 alpha-hydroxylation pathways in noninvolved human mammary tissue. The relative extent of estradiol 16 alpha-hydroxylation was found to be increased in TDLU from patients in the luteal phase of the menstrual cycle in relation to either those from patients in the follicular phase or from postmenopausal subjects. This study demonstrates that TDLU can metabolize estradiol extrahepatically and that 16 alpha-hydroxylation in the target tissue is dependent on the phase of the menstrual cycle. Furthermore, the specific, risk-related increase in 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, or a marker for, the relative risk of developing mammary cancer.

Aryl Hydrocarbon Hydroxylases↗
PubMed1992

The variability of the serum estradiol level in men: effect of stress (college examinations), cigarette smoking, and coffee drinking on the serum sex hormone and other hormone levels.

The results of studies carried out to evaluate the relationship of estradiol to coronary heart disease and its risk factors in men have been conflicting. Three possible causes of these conflicting results are (a) an inherent variability of the estradiol level within individual men; (b) the confounding effects on the estradiol level of certain common exogenous factors such as psychological stress, cigarette smoking, and coffee drinking; and (c) methodology and study design. The present study was conducted to test in men the inherent variability of the serum estradiol level and the effects of psychological stress (college examinations), cigarette smoking, and coffee drinking on the serum estradiol level. Subsets of 41 men, 19-57 years of age, were studied. A highly significant correlation in the estradiol levels was found between two fasting samples taken 30 minutes, 19.1 (mean) days, 2-6 months, and 10-89 months apart. Neither the stress of college examinations nor 30 minutes of cigarette smoking or coffee drinking had any apparent effect on the serum estradiol level, even in the presence of a two- to fivefold increase in the level of other hormones in four subjects with an autonomic reaction (three to smoking and one to venipuncture). It appears that the serum estradiol level is remarkably stable in men when taken under controlled conditions and that neither inherent fluctuation in this level nor the effects of the exogenous factors as studied are responsible for the conflicting results.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Effects of estradiol on platelet aggregation in mouse mesenteric arterioles and ex vivo.

Mice were implanted subcutaneously with a pellet containing 0.5 mg estradiol or with a placebo. Eight to 12 days later platelet aggregation was produced in mesenteric arterioles by injuring their endothelium in vivo with a noxious light/dye stimulus. The time between the onset of the noxious stimulus and the appearance of platelet aggregates was significantly shortened (p less than .01) in the estradiol treated mice. In contrast to this enhancement of aggregation, when platelets were tested ex vivo in platelet rich plasma (PRP), aggregation to sodium arachidonate was inhibited in estradiol treated mice. Aggregation of PRP by ADP was not affected by estradiol treatment of the mice. Thus the enhanced aggregation observed in injured mesenteric arterioles of estradiol treated mice may not reflect direct effects of estradiol on the platelet itself. Rather enhanced aggregation may reflect an effect of estradiol on endothelium or adjacent tissue. The data are discussed in light of other literature concerning estradiol effects in rodents, and in light of literature suggesting that an increased number of thromboembolic events occurs in humans receiving high doses of estrogens.

Adenosine Diphosphate↗
PubMed1983

Estradiol and tamoxifen stimulation of lapine articular chondrocyte prostaglandin synthesis.

The effect of estradiol and tamoxifen on prostaglandin (PG) synthesis by rabbit articular chondrocytes in secondary monolayer cultures was investigated. Radioimmunoassay for PGE2, PGF2 alpha, 6-oxo-PGF1 alpha and thromboxane B2 was performed on media from cultures containing estradiol and tamoxifen (10-12M-10-7M). Radiometric thin-layer chromatography was also carried out. The time course of estradiol/tamoxifen effect on chondrocyte PG synthesis was evaluated and its relationship to cell density in culture examined. Estradiol stimulated the synthesis of PGs by chondrocytes. Stimulation was noted at picomolar concentrations of estradiol without further stimulation at markedly higher concentrations. In time studies, after a lag, the effect of estradiol was present fully by 5 hrs, remained steady for 24 hrs and then declined by 48 hrs. Estradiol stimulation of PG synthesis was dependent upon chondrocyte culture plating density. Tamoxifen stimulated chondrocyte PG synthesis to relatively lower levels than estradiol. The characteristics of estradiol/tamoxifen stimulation of chondrocyte PG synthesis suggest a mechanism involving estradiol cytoplasmic receptors.

Animals↗
PubMed1987

The influence of estrous cycle and intrastriatal estradiol on sensorimotor performance in the female rat.

The influence of estrous cycle and intrastriatal implants of 17 beta-estradiol (17 beta-estradiol). 17 alpha-estradiol (17 alpha-estradiol) or cholesterol on the number of footfaults made by female rats traversing a narrow suspended beam was investigated. Female rats made fewer footfaults on estrus than on other days of the cycle. This was true when testing occurred during either the light or dark phase of the light:dark cycle. Intrastriatal implants of 30% 17 beta-estradiol for 6 hours resulted in a significant improvement in sensorimotor performance as soon as 4 hours after hormone implant and persisting for days. In contrast, intrastriatal implants of either 30% 17 alpha-estradiol or cholesterol had no influence on performance. The extent of hormone diffusion away from the implant cannula was minimal, and the resulting concentration of 17 beta-estradiol in the striatum was less than 10 pg/mg. It is concluded that estradiol has a direct, stereospecific effect in the striatum that influences performance of a skilled motor act in the female rat.

Animals↗
PubMed1986

Estradiol-induced alteration in the immune system. II. Suppression of cellular immunity in the rat is not the result of direct estrogenic action.

Estradiol has been reported to suppress numerous cellular immune response. What is not known is how estradiol exerts this effect. In vivo administration of estradiol to male rats caused time-related immunomodulatory effects leading to enhancement of lymphocyte transformation while suppressing a mixed lymphocyte reaction (MLR) response. The suppression of the MLR response was not due to alterations in the ratio of helper and suppressor T cells, nor was it due to alterations in either cell viability or the number of cells in culture. Lymphocytes cultured in vitro with estradiol, however, fail to show any alteration in the responsiveness in either MLR or lymphocyte transformation assays. The suppressive effects of estradiol cannot be transferred from a primary MLR culture to a second MLR culture using the supernatants from the primary MLR culture. Lymphocytes from animals given estradiol in vivo show no alteration in the production of interleukin 2: added in vitro to primary MLR cultures, Interleukin 2 failed to restore full responsiveness to lymphocytes from animals treated in vivo with estradiol. These results suggest that estradiol acts indirectly to cause an alteration in the responsiveness of the regulatory cells of the cellular immune system.

Animals↗
PubMed1989

Interleukin-1 suppresses follicle-stimulating hormone-induced estradiol secretion from cultured ovarian granulosa cells.

The effect of recombinant human interleukin-1 beta (IL-1 beta) on the follicle stimulating hormone-(FSH) induced secretion of estradiol was investigated using cultured granulosa cells obtained from immature rats with diethylstilbestrol implants. Estradiol secretion was significantly reduced by IL-1 beta in cultures containing FSH and either 10(-7) or 10(-8) M androstenedione as a substrate for estradiol synthesis. However, the inhibition of FSH-induced estradiol secretion by IL-1 beta was more apparent in the presence of 10(-8) M as compared to 10(-7) M androstenedione. IL-1 beta suppressed estradiol secretion during a 72 h culture in a dose-dependent manner with a minimum effective dose of 10 ng/ml. The reduction of FSH-stimulated estradiol secretion by IL-1 beta was greatest after a 48 h culture in the presence of 10(-8) M androstenedione. IL-1 beta did not effect estradiol production when cultures were incubated with various doses of androstenedione in the absence of FSH. Finally, IL-1 beta also suppressed the forskolin-induced secretion of estradiol. These results suggest that IL-1 beta may play some role in the multifactorial regulation of aromatase and estrogen secretion in the early developing follicle, and IL-1 beta may exert an effect on the cAMP-adenylate cyclase messenger system in granulosa cells. Taken together with previous studies, these results provide further evidence for the existence of a putative communications network between the immune and reproductive endocrine systems.

Androstenedione↗
PubMed1991

Effect of estradiol and progesterone on long chain fatty acyl-coenzyme A levels in the rat uterus.

Fatty acyl-CoAs are potential in vivo inactivators of glucose-6-phosphate dehydrogenase (G6PD). Ovariectomized mature rats (n = 74) were given 5 micrograms of estradiol intravenously, then killed 0, 24, 36, 48 and 72 h later. Control levels of myristoyl-, palmitoyl-, stearoyl-, arachidonoyl-, oleoyl- and linoleoyl-CoA were 0.6, 3.2, 4.7, 3.4, 2.4 and 3.0 micrograms/uterus and were increased 39, 110, 146, 100, 84 and 69% at 36-48 h, respectively. Levels of fatty acyl-CoAs in the rat uterus become elevated 36 h after estradiol treatment. At the same time G6PD changes from a stable enzyme to one that is irreversibly inactivated, possibly due to being rapidly degraded. Progesterone (2 mg subcutaneously every 12 h, n = 30), administered beginning at either 24 or 36 h after estradiol treatment, had no effect on estradiol-induced changes in myristoyl-, palmitoyl-, or stearoyl-CoA. Compared to the groups of rats treated with estradiol alone, animals treated with combinations of estradiol and progesterone exhibited higher levels of arachidonoyl-CoA after 48 h, and oleoyl-CoA and linoleoyl-CoA were greater after 72 h. Progesterone increased the estradiol-induced levels of unsaturated fatty acyl-CoAs suggesting that progesterone may induce uterine fatty acid desaturase activity and/or uptake of dietary fatty acids. Addition of fatty acyl-CoAs, at concentrations seen in vivo at 36-48 h after estradiol, to purified G6PD, causes irreversible G6PD inactivation.

Acyl Coenzyme A↗