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PubMed1977

Estradiol receptors and glucose-6-phosphate dehydrogenase activity in human breast tumors.

Estradiol receptors and glucose-6-phosphate dehydrogenase, an enzyme induced by estrogens, were measured in both benign and malignant human breast tumors. The mean glucose-6-phosphate dehydrogenase activity was higher in the malignant tumors than in the benign tumors. Tumors containing estradiol receptors contained higher activities of glucose-6-phosphate dehydrogenase than tumors without receptors. In breast carcinomas with and without estradiol receptors glucose-6-phosphate dehydrogenase gave 3 isoenzymes with very similar electrophoretic pattern after polyacrylamide gel electrophoresis. The results showed that although glucose-6-phosphate dehydrogenase was higher in estradiol receptor positive than in estradiol receptor negative tumors there was no significant correlation between the estradiol receptor concentration and glucose-6-phosphate dehydrogenase activity in human breast tumors.

Breast Neoplasms↗

PubMed1986

Peroxidase activity and estradiol receptors in human breast cancer.

In order to establish the relation between peroxidase activity in human breast carcinoma and its estrogen-dependency, estradiol receptors and their peroxidase activities were determined by a very sensitive fluorimetric method in 61 carcinomas. The geometrical mean of peroxidase activity in the 34 estradiol receptor negative carcinomas, 12.8 mU/g tissue, was significantly higher (p less than 0.05) than that of the 27 estradiol receptor positive cases, with a mean of 10.57 mU/g tissue. Necrosis and/or inflammation were found more frequently in the estradiol receptor negative carcinomas (p less than 0.01) than in the estradiol receptor positive. It is concluded that peroxidase activity is linked more to the typical biological behavior of the tumor than to tumoral estrogen-dependency. Thus, the estradiol receptor negative tumors, which showed a more aggressive behavior associated with frequent necrosis and intratumoral inflammatory signs, had a greater peroxidase activity.

Adult↗

PubMed1995

17beta-Estradiol inhibits the voltage-dependent L-type Ca2+ currents in aortic smooth muscle cells.

To elucidate the mechanisms of estrogens-induced relaxation effects on vascular smooth muscle cells, the effects of estrogens and the related hormones were examined in cultured rat thoracic aortic smooth muscle cell lines (A7r5), using the whole-cell voltage clamp technique. The patch pipette was filled with 140 mM CsCl- or KCl-containing internal solution. With CsCl-internal solution, 17beta-estradiol and synthetic estrogens, ethynylestradiol and diethylstilbestrol (0.1-30 mu M) inhibited the Ba2+ inward current (IBa) through the voltage-dependent L-type Ca2+ channel in a concentration-dependent and reversible manner. The potency of the inhibitory effects on IBa was 17beta-estradiol < ethynylestradiol < diethylstilbestrol. 17beta-Estradiol (10 mu M) appeared to reduce the maximal conductance of IBa with only a slight shift of voltage-dependency of inactivation and to affect IBa in a use-independent fashion. On the other hand, testosterone and progesterone (30 mu M) failed to affect IBa. At a holding potential of -40 mV, both vasopressin and endothelin-1 (100 nM) activated a long-lasting inward current. After endothelin-1 (100 nM) activated the current, the additional application of vasopressin (100 nM) could not induce it furthermore, suggesting that each agonist activates the same population of the channels. The reversal potential of the current was about 0 mV and was not significantly altered by replacement of [Cl-]i or [Cl-]0 and the inward current was also observed even when extracellular cations are Ca2+, proposing that it was a Ca2+-permeable non-selective cation channel (IN.S.). La3+ or Cd2+ (1 nM) completely abolished IN.S., however, nifedipine (10 mu M) failed to inhibit it at all. Diethylstilbestrol (1-30 mu M) suppressed the IN.S. evoked by both endothelin-1 and vasopressin in a concentration-dependent manner, while 17beta-estradiol, ethynylestradiol, progesterone and testosterone (30 mu M) failed to inhibit it significantly. In addition, at a holding potential of +0 mV, 17beta-estradiol by itself did not affect the holding currents, and did not inhibit K+ currents evoked by endothelin-1 or vasopressin, possibly due to the Ca2+ release from the storage sites. These results suggest that 17beta-estradiol may play a role in regulating vascular tone, selectively by inhibiting the voltage-dependent L-type Ca2+ current in vascular smooth muscle cells.

Animals↗

PubMed1983

Biphasic effect of estradiol and domperidone on lingual dyskinesia in monkeys.

In previous work, we demonstrated in animals and humans an antidopaminergic effect of estradiol at the level of the striatum. In the present study, we tested the effect of a large dose of estradiol (0.5 mg s.c.) administered either acutely or during several days in four female ovariectomized monkeys, displaying a persistent buccolingual dyskinesia due primarily to a midbrain lesion, but which is markedly enhanced by dopaminergic agonists. One of the monkeys also displayed a lesion-induced parkinsonian-like tremor of the opposite limbs. Chronic administration of estradiol markedly reduced the apomorphine-induced potentiation of the dyskinesia but did not affect the tremor. A single dose of estradiol was followed after 24 h by a 75% reduction of the effect of apomorphine on the dyskinesia but a 50% increase in the response to apomorphine was seen after 2 weeks. The response was at the control level after 30 days. Domperidone, a peripheral dopamine agonist that does not cross the blood-brain barrier and which causes an elevation of prolactin similar to that seen after estradiol, is followed by a similar biphasic modification of the response to apomorphine. Our results suggest that estradiol may have opposite effects on the sensitivity of the striatal dopamine receptors and therefore on dyskinesia, depending on the time of observation. An elevation of prolactin appears to have similar effects. Moreover, some effects of these hormones may be delayed by several days to weeks in primates.

Animals↗

PubMed1989

Estradiol-concentrating cells in the brains of hypogonadal female mice and in their intraventricular preoptic area implants.

Estradiol-concentrating cells were evaluated in the brains of hypogonadal female mice and in their intraventricular preoptic area brain grafts using autoradiography for [3H]estradiol. Normal distribution of estradiol-concentrating cells was observed in the brains of the hypogonadal mice with dense collections of these cells in the lateral septum; the medial preoptic area; the medial anterior hypothalamus; the ventromedial, arcuate, and periventricular nuclei of the hypothalamus; and the medial and cortical nuclei of the amygdala. In addition, estradiol-concentrating cells were present in all the transplants, with the estimated number of such cells in the transplants ranging from 390 to 2600. There was no correlation between numbers of estradiol-concentrating cells within the transplants and degree of reproductive recovery in the hypogonadal mice. Gonadotropin-releasing hormone (GnRH) immunocytochemistry of alternate sections revealed GnRH-immunoreactive material within the grafts and immunoreactive fibers exiting the grafts and entering the hosts' median eminence. No specific relationship between GnRH cells and estradiol-concentrating cells was evident within the grafts, nor was there any indication of identity of estrogen-concentrating cells with GnRH cells.

Animals↗

PubMed1991

Estradiol replacement to female rats facilitates dorsal hippocampal but not ventral hippocampal kindled seizure acquisition.

Estradiol replacement facilitates amygdala and neocortical kindling. This study determined if estradiol also interacts with kindling of additional limbic sites, the dorsal (dH) and ventral (vH) hippocampus. During dH stimulations, ovariectomized female rats with estradiol (E) replacement required 29.7 +/- 3.5 trials to kindle and accumulated 1170 +/- 90 s of afterdischarge (AD), significantly less than the 40.6 +/- 3.7 trials and 1620 +/- 225 s in rats without estradiol (nE). E did not significantly alter the long series of partial limbic seizures preceding generalized seizures despite the early appearance of AD in the contralateral amygdala. E significantly advanced the onset of generalized seizures compared to nE (22.7 +/- 2.3 versus 27.9 +/- 3.2 trials), an event coincident with neocortical AD development. Following secondary seizure generalization, E rats rapidly completed late-kindled seizure acquisition. In contrast, nE rats required an almost twofold greater number of AD trials and AD s to complete late kindling compared to E rats. One factor in the slower late kindling of nE rats was the instability of generalized seizures which frequently regressed to focal or partial responses. In marked contrast to dH kindling, vH kindling was uneffected by E replacement. The results provide further experimental evidence for a role for estradiol in catamenial epilepsy and support our previous work suggesting that the focal origin of seizure development is critical to E facilitation of kindling and that secondary generalization of seizures is especially sensitive to estradiol.

Animals↗

PubMed1983

Estradiol-17 beta and 17 alpha, 20 beta-dihydroxy-4-pregnen-3-one production by isolated ovarian follicles of amago salmon (Oncorhynchus rhodurus) in response to mammalian pituitary and placental hormones and salmon gonadotropin.

The effects of mammalian pituitary and placental hormones and dibutyryl cyclic AMP (cAMP) on the production of estradiol-17 beta and 17 alpha, 20 beta-dihydroxy-4-pregnen-3-one (17 alpha, 20 beta-diOHprog) by amago salmon (Oncorhynchus rhodurus) ovarian follicles in vitro were compared with partially purified chum salmon (Oncorhynchus keta) gonadotropin (SGA). Estradiol-17 beta production was examined using midvitellogenic ovarian follicles; SGA was the most effective hormone tested; at a dose of 1 microgram/ml it stimulated the production of approximately 4 ng/ml estradiol-17 beta. Ovine LH (o-LH) was about 0.5% as effective as SGA. Taking into account the relative purity of the preparations used, ovine FSH (o-FSH) was almost as effective as o-LH. Both HCG and bovine TSH (b-TSH) stimulated estradiol-17 beta production at high doses. Porcine ACTH (p-ACTH), ovine GH (o-GH), and ovine PRL (o-PRL) induced very modest increases in estradiol-17 beta; cAMP was highly effective. 17 alpha, 20 beta-DiOHprog production was examined using full-grown immature oocytes which were capable of maturing in vitro in response to 1 microgram/ml SGA. o-LH was about 0.5% as effective as SGA. o-FSH, b-TSH, and HCG appeared to be less effective in stimulating 17 alpha, 20 beta-diOHprog production, compared to estradiol-17 beta. o-GH and o-PRL induced marginal increases in production and p-ACTH had a very modest inverse dose-response effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1986

Effect of plasma lipoproteins in gonadotropin stimulation of 17 beta-estradiol production in the ovarian follicle of rainbow trout (Salmo gairdneri).

The effect of trout plasma lipoproteins on the production of 17 beta-estradiol by trout ovarian follicles is investigated in vitro. 17 beta-Estradiol secretion into the medium was assayed as a function of follicular diameter in the presence of lipoproteins with and without salmonid gonadotropin (SGA-GTH). The presence of very low-density lipoproteins (VLDL) + chylomicrons (Chy), low-density lipoproteins (LDL), and high-density lipoproteins (HDL) amplified the SGA-GTH effect at the lowest concentrations tested (less than 50 micrograms protein/ml). HDL is the most effective for increasing hormone accumulation on a microgram lipoprotein sterol basis. Autoradiography of 125I-labeled LDL showed that they were preferentially bound by thecal cells. Kinetics of 17 beta-estradiol release indicated that lipoprotein amplification occurred especially after 15 hr and subsequent metabolism of 17 beta-estradiol by follicular layers also led to an equilibrium. At the end of vitellogenesis apoprotein B lipoproteins (VLDL + Chy, LDL) apparently inhibited SGA-GTH stimulation. N',O'-Dibutyryl cAMP (10 mM) considerably stimulated 17 beta-estradiol production but lipoprotein amplification did not occur. Chloroquine (30 microM) inhibition of LDL and HDL amplification indicates that this process requires lysosomal degradation. Plasma lipoproteins in trout modulate SGA-GTH stimulation of 17 beta-estradiol production during exogenous vitellogenesis. Due to the ease and frequency with which the experiments can be carried out, the ovarian follicle of salmonids is an excellent model for the study of the role of lipoproteins in the regulation of ovarian steroids biosynthesis.

Animals↗

PubMed1987

Estradiol-17 beta Silastic implants suppress oocyte development in the brook trout, Salvelinus fontinalis.

A technique for long-term implantation (i.e., 6 months) of steroid-containing Silastic capsules in brook trout was developed along with a method for longitudinal study of ovarian dynamics in individual females. Estradiol-17 beta implantation, extending from spring during early oogenesis through November, suppressed overall ovarian development in a dose-dependent manner, as determined by follicle size analysis and gonosomatic index, and reduced the peak of plasma estradiol-17 beta normally observed prior to ovulation in the fall. Frozen sections of follicles revealed that estradiol implants retarded the progression of vitellogenesis from primary to secondary stages in the largest size class of follicles. In particular, sections of ovarian biopsies from animals with three estradiol implants had only small follicles in September which cytologically were no more advanced than those in May. By contrast, animals receiving steroid-free implants had significantly larger follicles in September which entered the secondary stage of vitellogenesis and became increasingly competent to respond to progestogen treatment in vitro through October and November. Image analysis of ovarian biopsies indicated that estradiol implants deranged the normal group-synchronous growth pattern of the brook trout ovary and tended to produce asynchronous growth, especially in animals with a single estradiol implant.

Animals↗

PubMed1989

Estradiol-17 beta silastic implants in female Rana ridibunda depress thyroid hormone concentrations in plasma and the in vitro 5'-monodeiodination activity of kidney homogenates.

Estradiol-17 beta containing silastic tubings were implanted in female Rana ridibunda. Preliminary data, concerning in vitro incubations of such tubings in saline media, revealed that high concentrations of estradiol were released out of the tubings in the incubation medium. Compared to control-implanted frogs, the frogs that had the estradiol tubings implanted for 30 days showed a significant increase of the plasma estradiol concentration, the ovarian estradiol concentration, and the weight of the oviduct. Plasma triiodothyronine (T3) levels, plasma thyroxine levels, and the in vitro T3 production in the kidney homogenates were significantly decreased. These results indicate that high estradiol levels not only influence the gonadal axis, but also cause important effects on the thyroidal axis.

Animals↗

PubMed1988

Progesterone facilitation of lordosis in male and female Sprague-Dawley rats following priming with estradiol pulses.

Adult male Sprague-Dawley rats rarely exhibit progesterone-facilitated lordosis following steroid treatments which are effective in females. In contrast, progesterone-facilitated lordosis has been observed following priming with estradiol pulses in another strain. The aim of this study was to compare progesterone-facilitated feminine sexual behavior in adult male and female Sprague-Dawley rats following priming with estradiol benzoate (EB) or estradiol pulses. Female sexual behavior was measured in adult, gonadectomized males and females treated as follows: Two pulses of estradiol followed by progesterone or oil the next day; EB (two doses) for 3 days, and progesterone or oil the next day. These protocols were repeated at 4- or 6-day intervals, respectively. Progesterone-facilitated lordosis was observed consistently in both sexes treated with estradiol pulses. By the fifth test, lordosis quotients did not differ between the sexes, but the lordosis ratings in progesterone-treated males remained lower than those observed in females. Proceptivity (hop-darting) was facilitated by progesterone in females, but was never observed in males. Lordosis was induced in both sexes by 15 micrograms EB, but was not reliably facilitated by progesterone. Treatment with the lower dose of EB (1.5 micrograms) induced high levels of receptivity in females (occasionally facilitated by progesterone), but not in males regardless of subsequent treatment (i.e, progesterone or oil). These data suggest that progesterone-facilitated lordosis can be induced in male Sprague-Dawley rats, if a regimen of estradiol pulses is used. Thus, the brain of the adult male is not inflexibly differentiated with regard to progesterone facilitation of feminine receptive behavior.

Animals↗

PubMed1979

Novel enzyme immunoassay for 17 beta-estradiol.

A novel approach to the enzyme immunoassay of analytes is presented and illustrated by demonstration of an estradiol assay. The assay depends on the competitive binding of estradiol and estradiol-DNP conjugate to immobilized anti-estradiol. The amount of estradiol-DNP bound is inversely proportional to the amount of free estradiol, and is measured through the use of peroxidase-labeled anti-DNP antibodies. The assay gives a dose-response curve from 10 pg/tube to 450 pg/tube and shows satisfactory correlation with radioimmunoassay.

Estradiol↗

PubMed1982

Calculation of free and bound fractions of testosterone and estradiol-17 beta to human plasma proteins at body temperature.

A mathematical model for the calculation of free and protein bound concentrations of testosterone and estradiol in plasma is presented. The method is based on the knowledge of the total concentrations of all steroids competing for the same binding site on testosterone-estradiol-binding globulin (TeBG), the concentration of albumin, the binding capacity of TeBG, and the association constants of the steroids to the two binding proteins. For the calculations we have determined the total concentrations of testosterone and estradiol. TeBG binding capacity, albumin concentration and the association constants for the binding of testosterone, estradiol and 5 alpha-dihydrotestosterone (DHT) to TeBG and albumin at 37 degrees C. Physiological concentrations of some androgen metabolites reported in the literature were also included in the calculations, namely: DHT, 5-androstene-3 beta, 17 beta-diol (Ae) and 5 alpha-androstane-3 alpha, 17 beta-diol (Aa). The binding constants for Ae and Aa to TeBG and albumin were also from the literature. Mean values of testosterone were calculated for 11 normal men and expressed as percentages of total: 2.0% was unbound, 53--55% bound to albumin and 43--45% bound to TeBG. For 16 normal women of a fertile age the corresponding values were 1.5%, 36--37% and 62%. For estradiol they were 2.4% 68--70% and 28--30% in the men and 2.0%, 52% and 45--46% in the women. Variations in the concentrations of DHT. Ae and Aa did not influence the free concentrations of testosterone and estradiol to any significant extent. It was furthermore concluded that the androgen metabolites could be omitted from the calculations without affecting the calculated concentrations.

Adult↗

PubMed1986

Radiochemical evidence for estradiol-17-fatty acid esters in human blood.

The C-17 fatty acid esters of estradiol, known as the lipoidal derivatives of estradiol, LE2, are metabolites of estradiol that were originally isolated from various tissues after in vitro incubations with estradiol. These steroidal esters are active estrogens with extremely prolonged potencies. The present study investigates the existence of LE2 in human blood using a radiochemical isotope dilution technique. The LE2 fraction from blood was isolated, saponified, and the hydrolyzed estradiol was then acetylated with [3H]acetic anhydride. It was found that 3H was incorporated into estradiol diacetate, demonstrating that LE2 is present in human blood. Thus these steroidal esters represent a new class of endogenous estrogens which have not been previously considered in the physiology of the female sex steroids.

Acetic Anhydrides↗

PubMed1989

Formation of glucuronides of estradiol-17 beta by human mammary cancer cells.

The formation of glucuronides of estradiol-17 beta by human mammary cancer cell lines is reported for the first time. When incubated with [3H]estradiol-17 beta (1 nM) for 16 h, ZR-75-1 and T47-D cells formed estradiol-3-glucuronide and estradiol-17 beta-glucuronide in approximately equal proportions, whereas MCF-7 cells formed E2-3-glucuronide only. Yields of monoglucuronides from MCF-7 and ZR-75-1 cells were 0.35 pmol/mg DNA, which represented 20-26% of the yield of estradiol-monosulphates. A HPLC system capable of separating most estradiol monosulphates, monoglucuronides and mixed conjugates, is described.

Breast Neoplasms↗

PubMed1983

Effect of porcine relaxin and estradiol-17 beta on the incorporation of tritiated thymidine by fibroblasts isolated from guinea pig uteri.

Fibroblasts isolated from the uteri of 5 guinea pigs were cultured in vitro to determine the effect of relaxin and estradiol. Both relaxin and estradiol increased thymidine uptake by fibroblasts. Thymidine incorporation with 1.5 micrograms/ml relaxin and no estradiol was 107% of control while 600 pg/ml estradiol and no relaxin gave 112% of control. Thymidine incorporation in the presence of 1.5 micrograms/ml relaxin and 600 pg/ml estradiol was 128% of control. This indicated a significant interaction between relaxin and estradiol.

Animals↗

PubMed1994

Selection of a highly tumorigenic breast cancer cell line sensitive to estradiol to evidence in vivo the tumor-inhibitory effect of butyrate derivative Monobut-3.

To increase butyric acid mean residence time in vivo, we have produced a stable butyric acid derivative. Monobut-3. Recently, we have described that Monobut-3 is able to induce phenotypic changes in human mammary tumor cells in vitro. In this study, we explore the in vivo effect of Monobut-3. Human breast tumor cell-lines did not easily produce in vivo xenografts, thus, MCF-7 cells required exogenous 17 beta-estradiol to grow and to form in vivo xenografts. To evaluate in vivo and anti-tumor effects of monobut-3 without exogenous 17 beta-estradiol addition, we have established MCF-7 variant cells, highly tumorigenic MCF-7vht, in which transfection of ras oncogene induced a bypass of estrogen requirement but did not delete the presence of functional estrogen receptor (ER). Monobut-3 inhibited growth of this variant by about 90% at 4 mM and reduced 17 beta-estradiol cell growth stimulation. In vivo, in absence of 17 beta-estradiol, 2 mg per mouse monobut-3 decreased tumor take by about 25% and tumor growth by about 50% in nude mice. This is the first experimental demonstration of an in vivo antitumoral effect of a butyric acid derivative alone on a solid human tumor. These data suggest that this compound does not only act by reducing of 17 beta-estradiol stimulation but it also has an 17 beta-estradiol-independent effect. Absence of toxicity and its antiproliferative effects could suggest its use in clinical treatment of well differentiated carcinoma.

Animals↗

PubMed1991

Intranasal estradiol administration to oophorectomized women.

An open, dose-finding study into the effects of a new intranasal 17 beta-estradiol formulation using dimethyl-beta-cyclodextrin as a solubilizer was conducted in nine hysterectomized and oophorectomized patients with symptoms of estrogen deficiency. After nasal delivery of 0.34 mg estradiol in three patients, concentration-time curves of estradiol in serum and its metabolite estrone in plasma were established. High initial estradiol serum levels were found in the order of 5 nmol/l. Estrone/estradiol ratios were below unity, whereas, in contrast, estrone/estradiol ratios after oral administration of estradiol are known to exceed unity. Biological activity, as reflected by suppression of FSH and LH, was manifest. In nine patients symptoms of estrogen deficiency were assessed by a questionnaire. After 3 and 6 months of treatment, a clinically and statistically significant decrease (P less than 0.01) of the total score according to this questionnaire was found compared to the beginning of the study. Thus nasal delivery of estradiol using this cyclodextrin formulation has potential for further clinical evaluation.

Administration, Intranasal↗