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PubMed1991

Electrophysiological evidence for a rapid membrane action of the gonadal steroid, 17 beta-estradiol, on CA1 pyramidal neurons of the rat hippocampus.

The rapid electrophysiological effects of 17 beta-estradiol on CA1 pyramidal neurons (n = 86) were investigated utilizing intracellular recording from the rat hippocampal slice preparation. Bath application of 17 beta-estradiol, but not 17 alpha-estradiol, caused a reversible depolarization and increased input resistance with a latency of less than 1 min in 19.8% of CA1 neurons tested. There was no significant difference in the percentage of estradiol-responsive cells between male and female rats. Estradiol-responsive cells were identified from prepubertal female rats, as well as females in all stages of the estrous cycle. 17 beta-estradiol had no effect on the slow afterhyperpolarization or accommodative properties of CA1 neurons. In 2 out of 4 cells tested, the specific antiestrogen, tamoxifen, blocked the excitatory response to 17 beta-estradiol.

Animals↗
PubMed1991

Different hepatobiliary effects of oral and transdermal estradiol in postmenopausal women.

Estrogen-replacement therapy is important for the prevention of postmenopausal osteoporosis. However, oral synthetic and conjugated estrogens increase biliary cholesterol saturation index and risk of gallstone disease. To examine whether transdermal estrogen administration could avoid these adverse effects, 17 postmenopausal women were treated with transdermal estradiol (Estraderm TTS; Ciba-Geigy, Arnhem, The Netherlands), 100 micrograms/day for 4 weeks, and after 1 month without therapy, with oral estradiol (Progynova; Schering, Weesp, The Netherlands), 2 mg/day for 4 weeks. The increase in the serum estradiol level was much higher during transdermal than oral estradiol administration. On the contrary, the increase in the serum estrone level was much more pronounced during oral treatment. Both modes of treatment led to a similar reduction of urinary calcium excretion. A highly significant decrease in serum phosphate levels was found during transdermal therapy. Biliary cholesterol saturation index did not change during transdermal therapy (mean +/- SEM, 1.25 +/- 0.06 before and 1.22 +/- 0.07 at the end of transdermal therapy; P = NS). A slight increase in cholesterol saturation index that did not reach statistical significance was found during oral therapy (1.28 +/- 0.09 before and 1.36 +/- 0.09 during oral treatment). However, the subgroup of women with strong increases in serum estrone levels during oral estradiol therapy (greater than 0.5 pmol/mL; n = 8) generally had increased biliary cholesterol saturation index, a decrease in relative percentage chenodeoxycholic acid in bile, and increased serum sex hormone-binding globulin levels during oral treatment. Cholesterol monohydrate crystals were never found in duodenal biles during either treatment. This study indicates that transdermal estradiol does not induce lithogenic bile. On the contrary, oral estradiol leads to lithogenic bile in a subgroup of women with strong increases in serum estrone levels during oral treatment.

Administration, Cutaneous↗
PubMed1986

The in vitro effects of cyclic nucleotides, cyanoketone, and cycloheximide on the production of estradiol-17 beta by vitellogenic ovarian follicles of goldfish (Carassius auratus).

The effects of human chorionic gonadotropin (HCG), forskolin, cyclic nucleotides, the phosphodiesterase inhibitors IBMX and theophylline, cyanoketone, and cycloheximide on the production of estradiol-17 beta by isolated ovarian follicles of vitellogenic goldfish (Carassius auratus) were examined using 18-hr incubations. HCG and all test agents which are known to increase intracellular concentrations of cAMP significantly stimulated the production of estradiol-17 beta. However, dibutyryl cGMP was unable to stimulate estradiol-17 beta production at any concentration used (1-10 mM). Cyanoketone at a concentration of 1 micrograms/ml completely blocked forskolin-induced estradiol-17 beta production. Even in the presence of cyanoketone, however, forskolin stimulated conversion of exogenous testosterone to estradiol-17 beta in a dose-dependent manner, suggesting the involvement of an adenylate-cyclase system in the induction of aromatase activation by vitellogenic follicles of goldfish. Cycloheximide also completely abolished HCG-induced estradiol-17 beta production when this inhibitor was added within the first 1 hr after the addition of HCG. These results provide evidence that the stimulation of estradiol-17 beta by goldfish vitellogenic follicles in response to HCG is dependent upon the synthesis of new protein.

1-Methyl-3-isobutylxanthine↗
PubMed1986

Glucosidation of estradiol-17 beta in the cultured ovaries of the silkworm, Bombyx mori.

Metabolic pathways of estradiol-17 beta and other vertebrate steroid hormones of cultured silkworm pupal ovaries were examined using 14C-labeled steroids. The isolated ovaries showed significant uptake and metabolic activity of the 14C-labeled estradiol-17 beta added to the medium. Analysis of the metabolized compounds by thin-layer chromatography (TLC) and high-performance liquid chromatography (HPLC) revealed extensive metabolic conversion of [14C]estradiol-17 beta and estrone; i.e., estrone was reduced to estradiol-17 beta and estradiol-17 beta was metabolized to conjugates, including estradiol-3-beta-D-glucoside and estradiol-17-alpha-D-glucoside. [14C]Testosterone was not transformed appreciably by the ovaries. Metabolic activity and physiological significance of the vertebrate steroid hormones in the silkworm ovaries are discussed.

Animals↗
PubMed1990

Estradiol administration and the sexual activity of castrated male rhesus monkeys (Macaca mulatta).

To examine whether estradiol might be effective in maintaining sexual behavior after castration or after testosterone withdrawal, we have observed male rhesus monkeys during daily 1-hr tests alternately with each of two ovariectomized, estradiol-treated females (four males, four females, eight male-female pairs, 798 tests). Estradiol (2-5 micrograms/kg sc/day) or vehicle was administered in counterbalanced order immediately after castration and again immediately after withdrawal of testosterone propionate treatments (800 micrograms and 1.6 mg sc/day). There were no significant differences in behavior during vehicle and estradiol treatments to indicate that estradiol helped to maintain male sexual activity. Instead, estradiol treatment tended to interfere with the capacity to intromit. This supported the results of other studies, namely, that the systemic administration of estradiol does not enhance the sexual behavior of castrated male macaques, and raises questions about the role of both aromatization and estrogen receptors in the male primate brain.

Animals↗
PubMedDate not supplied

Estradiol-binding sites in rat aortic smooth muscle cells in culture.

To determine whether aortic smooth muscle cells possess estradiol receptors or not, an estradiol binding study has been performed in cultured rat aortic smooth muscle cells by using an intact-cell assay. Specific binding for estradiol is shown by the cells, and the binding reaches a plateau after 15 min of incubation at 37 degrees C. The binding curve shows a saturable binding process. Scatchard analysis reveals a single population for estradiol binding with a dissociation constant of 5.0 X 10(-8) M and specific binding sites of 64 fmole per 10(6) cells (38,500 sites per cell). Molecular specificity shows highly specific binding with estradiol. Among various steroids tested, only testosterone at 10(-5) M competes slightly (9.3%) with the estradiol-specific binding. These data indicate the existence of specific, high-affinity and limited-capacity binding sites for estradiol in rat aortic smooth muscle cells. This accords with the concept that estrogen responsiveness in aortic smooth muscle cells is mediated through the estrogen-receptor binding in the cells.

Animals↗
PubMed1993

Protective effect of 17 beta-estradiol against the cytotoxicity of minimally oxidized LDL to cultured bovine aortic endothelial cells.

The ability of 17 beta-estradiol, progesterone, testosterone and cholesterol in preventing the cytotoxicity of oxidized LDL to cultured aortic bovine endothelial cells (BAEC) was tested and compared. The lipid peroxidation of LDL, promoted either by UV-C radiation, copper ions or cultured human lymphoblastoid cells, was inhibited in a dose-dependent manner by 17 beta-estradiol (IC50 were evaluated at around 50 +/- 10 mumol/l with UV on copper and 6 +/- 2 mumol/l with cells), whereas exogenous cholesterol, progesterone or testosterone were completely inactive under the range of concentrations tested (up to 100 mumol/l). Subsequently, this antioxidant effect of 17 beta-estradiol preventing LDL oxidation protected 'indirectly' BAEC against the cytotoxicity of oxidized LDL. 17 beta-Estradiol was also able to protect 'directly' BAEC against the cytotoxic effect of oxidized LDL (with an IC50 around 0.5 +/- 0.1 mumol/l), whereas the other steroids tested were almost completely inactive. This direct protective effect resulted from an increased resistance of BAEC against the cytotoxic effect of oxidized LDL as shown by pre-incubation of BAEC with 17 beta-estradiol. The protective effect of 17 beta-estradiol was present for 2-3 days. In conclusion, 17 beta-estradiol exhibited an antioxidant activity and was effective in protecting BAEC against the cytotoxicity of oxidized LDL by acting at two separate sites: (i) outside the cells, by inhibiting the LDL oxidation; (ii) inside the cells by increasing the cellular resistance against the cytotoxic effect of oxidized LDL. The potential relevance of these results in relation to prevention of atherogenesis is discussed.

Animals↗
PubMed1985

Synthesis and biological assessment of long-acting estradiol fatty acid esters in ovariectomized rats.

Diesters of 17 beta-estradiol using palmitic acid (16:0) and oleic acid (18:1, cis-9-Octadecenoic acid) have been synthesized for potential evaluation as long-acting compounds. Female castrated rats were injected 1 mumol of estradiol dipalmitate and estradiol dioleate, using estradiol benzoate and estradiol enanthate as controls. Biological activity was determined by uterine wet weight and uterine diameter as well as on the suppression of serum anterior pituitary gonadotropins. A delayed absorption of estradiol was observed after administration of both diesters which was well correlated with the duration of biological effects. The data demonstrate that esterification with palmitic or oleic acids at 3 and 17 positions provides long-acting properties to 17 beta-estradiol, which could be applied in substitutive therapy and or in hormonal contraception.

Animals↗
PubMed1988

Correlations between free plasma estradiol and estrogens determined by bioluminescence in saliva, plasma, and urine during spontaneous and FSH stimulated cycles in women.

Estrone and estradiol (E1 + E2) concentrations in saliva were compared with four other parameters of estrogen status in five normal ovulatory women and ten FSH stimulated women selected for an in vitro fertilization program. E1 + E2 in saliva, plasma, and urine were assessed by a rapid, specific and sensitive enzymatic assay using bioluminescence. The free fraction of plasma estradiol was determined by equilibrium dialysis and total plasma estradiol by conventional radioimmunoassay. The pattern of E1 + E2 variation in saliva was similar to that of free plasma estradiol and the two parameters were correlated in both spontaneous and stimulated cycles. However, the lower correlation coefficient (r = 0.52, P less than 0.001) in spontaneous cycles compared with the high (r = 0.96, P less than 0.001) in the stimulated cycles shows that salivary E1 + E2 could be representative of plasma free estradiol in stimulated cycles but not in normal cycles. The free fraction of plasma estradiol reproduced the variation of total plasma estradiol in spontaneous as well as in FSH stimulated cycles and both parameters were strongly correlated (r = 0.91, P less than 0.001 and r = 0.90, P less than 0.001), respectively. The data show that salivary E1 + E2 concentrations are highly representative of the free fraction of E2 in plasma and at a lesser extend (r = 0.72, P less than 0.001) of total plasma E2 in FSH stimulated cycles.

Adult↗
PubMed1990

Modulation of quail oviduct adenylate cyclase activity by estradiol and progesterone.

Oviduct adenylate cyclase activity of the quail was measured by radiochemical analysis following different hormonal treatments. A single injection of estradiol benzoate (EB) to immature female quails resulted in a prereplicative surge of adenylate cyclase activity. A second surge of enzyme activity was observed during the proliferative phase induced by EB. Estradiol-17 alpha, estrone, estriol and testosterone were ineffective. Tamoxifen completely inhibits the growth-promoting effect of EB and the second surge of adenylate cyclase activity but does not inhibit the prereplicative increase of enzyme activity. This prereplicative increase of adenylate cyclase activity was also observed, even in the absence of increased plasma estradiol, when estradiol-17 beta (E2) was perfused through the hepatic portal vein. Moreover, E2 had no effect on enzyme activity when added directly to the oviduct homogenate preparation, at concentrations ranging from 10(-9) to 10(-7) M. In response to progesterone injection, oviduct adenylate cyclase activity followed a different pattern, beginning its increase after 3 h and remaining elevated up to 24 h. The activation by estradiol was independent of the presence of guanylylimidodiphosphate. Moreover, the enzyme was more sensitive to forskolin at submaximal concentration in estradiol treated birds than in control. These results demonstrate that transient activation of adenylate cyclase at the early stages of the action of estradiol does not occur through the classic nuclear receptor-gene activation pathway or a membrane receptor mediated process, but involves an indirect pathway, yet to be defined.

Adenylyl Cyclases↗
PubMed1985

Regulation of beta-endorphin and ACTH in brain by estradiol.

The effect of estradiol on the brain concentration of immunoreactive beta-endorphin (beta-EP) and C-terminal ACTH (CLIP) was studied in ovariectomized rats. Dopamine, a known inhibitor of pituitary intermediate lobe pro-opiomelanocortin (POMC), was examined as a possible mediator of the estradiol induced changes in brain POMC. Animals were treated for 1 or 3 weeks with either 1) saline; 2) silastic estradiol implants; or 3) estradiol implants plus haloperidol 1 mg/kg/day. After one week of treatment no significant change in hypothalamic beta-EP content was noted in any group compared to the control level of 4.13 +/- .33 (SEM) pmoles although in the neurointermediate lobe beta-EP increased from 566 +/- 72 to 942 +/- 73 pmoles after haloperidol (p less than .005). After 3 weeks, however, hypothalamic beta-EP decreased from 3.96 +/- .28 to 2.74 +/- .19 pmoles (p less than .005) and C-terminal ACTH decreased from 3.78 +/- .33 to 2.82 +/- .18 pmoles (p less than .02) in the estradiol treated rats. This estradiol induced decrease in the hypothalamic content of beta-EP and C-terminal ACTH was not blocked by haloperidol. We conclude that estradiol lowers the hypothalamic content of beta-EP and CLIP and that this effect does not appear to be mediated by dopamine.

Adrenocorticotropic Hormone↗
PubMed1992

The effects of estradiol on pituitary responsiveness to dopamine in vitro: a comparison of ovariectomized Fischer 344 and Holtzman rats.

The objective of this study was to determine if the effectiveness of dopamine as an inhibitor of prolactin is altered by estradiol in strains of rats which show marked differences in estrogen-induced pituitary hyperplasia. Groups of Fischer 344 and Holtzman Sprague-Dawley rats were ovariectomized and implanted with Silastic capsules of estradiol. Rats were sacrificed by rapid decapitation following a brief period of ether anesthesia at 2, 4, 6, 8 weeks (F-344) or at 2 and 8 weeks (Holtzman) of estradiol treatment. The pituitary was removed and cut into fragments which were either snap frozen for initial prolactin content measurements or incubated for 60 min in the presence or absence of dopamine (1 x 10(-6) M). Prolactin was measured in the plasma, in sonicates of the pituitary and in the incubation medium by double antibody radioimmunoassay. Pituitary weight and plasma levels of prolactin were significantly less in Holtzman rats compared to Fischer 344 females at 2 or 8 weeks of estradiol treatment but pituitary concentrations of prolactin were not different between the two strains. Pituitary fragments from Fischer 344 rats studied at 2 and 4 weeks of estradiol treatment did not respond to the removal of dopamine in vitro whereas pituitary fragments from Holtzman rats obtained at 2 weeks of estradiol treatment did release significantly more prolactin in the absence than in the presence of dopamine. Pituitary fragments taken from Fischer 344 rats at 6 and 8 weeks were responsive to dopamine whereas pituitary tissue from Holtzman rats was not responsive at 8 weeks. The data indicate that temporal differences in responsiveness to the inhibitory effects of dopamine occur in strains which are susceptible or resistant to the formation of pituitary tumors following prolonged estradiol treatment.

Analysis of Variance↗
PubMed1983

Behavioral and cellular responses to pulses of low doses of estradiol-17 beta.

The effectiveness of single vs. separate pulses of low doses of free estradiol on the induction of sexual receptivity in ovariectomized female rats was examined. Two separate subcutaneous pulses of low doses of free estradiol at 0 and 6 hours induced high levels of progesterone facilitated receptivity at 24 hours. However, a single pulse of the same total dose of estradiol induced little or no receptivity at 24 hours (or at 18 hours). In fact, approximately 10 times as much estradiol was required in a single pulse to induce comparable receptivity. The smaller behavioral response to a single pulse was not likely due to a ceiling effect or an unutilized excess of the hormone after one injection. This suggestion is based on measurements of the redistribution of estrogen receptors from the cytoplasm to cell nuclei as an index of an initial cellular stimulus. Doses of estradiol used in the behavioral studies included several doses that were subsaturating with regard to hypothalamic estrogen receptors. The greatly enhanced behavioral response to two separated pulses of estradiol is consistent with the hypothesis that an initial action of estradiol may be to sensitize target tissues to further stimulation by the hormone.

Animals↗
PubMed1995

Estradiol interacts with gastric or postgastric food stimuli to decrease sucrose ingestion in ovariectomized rats.

The sham feeding preparation was used to determine whether systemic estradiol administration inhibits the intake of 0.8 M sucrose of ovariectomized rats by decreasing the potency of pregastric controls of ingestion. During real feeding, significant reductions in the sucrose intake of estradiol-treated rats appeared within 5-6 min. In contrast, estradiol had no effect on sham feeding at any time. The lack of effect of estradiol on sham feeding indicates that pregastric stimuli are not sufficient to mediate the inhibitory effect of estradiol on feeding in ovariectomized rats. Rather, because estradiol did inhibit real feeding, gastric and/or postgastric food stimuli are necessary for this inhibitory effect. The rapid onset of estradiol's inhibitory effect on real feeding suggests that these postingestive stimuli are selective for controls of the initial phase of the meal.

Animals↗
PubMed1976

Metabolites of estradiol-17beta in guinea pig uterus late in pregnancy.

The metabolism of estradiol-17beta by the guinea pig uterus late in pregnancy was studied in vivo and in vitro. Whole uteri were examined for estrogen metabolites one hour following an intravenous injection of [3H]-estradiol-17beta or uterine sections were examined after incubation for one hour at 37 degrees C in medium containing [3H]-estradiol-17beta. In both instances uterine tissue metabolized estradiol-17beta to five products; estrone, estrone-3-sulfate, 17beta-estradiol-3-sulfate, estrone-3-glucuronide and 17beta-estradiol-3-glucuronide. Of the total radioactive products 11-43% were glucuronides, 17-26% were sulfates and 4-17% was estrone. These results indicate that the guinea pig uterus actively transforms estradiol-17beta into glucuronides and sulfates late in pregnancy.

Animals↗
PubMed1976

Effect of hypophysectomy on estrogen conjugation and on plasma and tissue concentrations of tritium after administration of 3H-estradiol-17beta.

Estradiol-17beta-6,7-3H was injected into ovariectomized (control) and ovariectomized, hypophysectomized (hypox) rats in order to study the binding of estradiol in the brain. Hypophysectomy resulted in a significant increase in the concentration of tritium in the hypothalamus, and preoptic area, as well as cortex, muscle, plasma and liver. However, since the liver was lighter in hypox rats, the total tritium content in the liver was unchanged from controls. Part of the weight reduction in the liver was due to a loss of stainable glycogen, which took place within 24 hours of hypox. The increase in circulating tritiated estradiol after hypox led us to investigate hepatic metabolism of estradiol. In vitro studies on liver slices from control and hypox rats demonstrated a significant reduction in the formation of conjugates of estrogen. Specifically, estradiol glucuronide and estrone sulfate formation were reduced in hypox rats and conversely the unmetabolized estradiol concentration was higher. Hypophysectomy for 24 hours results in a significant decrease in hepatic metabolism of estradiol-17beta.

Animals↗
PubMed1990

The effect of smoking on serum progesterone, estradiol, and luteinizing hormone levels over a menstrual cycle in normal women.

Since smoking has been shown to affect serum progesterone and estradiol levels in postmenopausal women, we evaluated the levels of these hormones and luteinizing hormone (LH) over an entire menstrual cycle (17 points) in eight healthy nonsmokers and eight healthy smokers. The total length of the cycle and the lengths of the follicular and luteal phases did not differ between the groups. There was no difference in estradiol, progesterone, or LH levels during the periovulatory and luteal phases. Follicular-phase serum progesterone, which had a level 37% higher in smokers, showed a plateau in both groups (28.3 +/- 5.7 ng/dl versus 20.7 +/- 5.7; P less than 0.0001). Follicular-phase serum estradiol showed a rising curve in both groups. The mean value in smokers was slightly higher than that in nonsmokers (107 pg/ml versus 95; P approximately 0.05); during the early part of the follicular phase, prior to the rapid preovulatory increase, the difference was greater (23%) and of higher statistical significance (80 pg/ml versus 65; P less than 0.001). The follicular-phase LH levels of smokers were skewed downward from the levels in nonsmokers, presumably by negative feedback from the elevated estradiol and progesterone levels; the difference was significant (P less than 0.001). The elevations of serum progesterone and estradiol in smokers probably represent activation of adrenocortical secretion by smoking. The greater and more clear-cut rise of progesterone than of estradiol is probably due to the fact that essentially all of the follicular-phase serum progesterone is secreted by the adrenal, while only part of the follicular-phase serum estradiol comes from the adrenal (via androstenedione and estrone).

Adult↗
PubMed1987

Acquisition of amygdala-kindled seizures in female rats: relationship between the effect of estradiol and intra-amygdaloid electrode location.

Ovariectomized, adult female rats, with or without estradiol replacement, were kindled by daily amygdala stimulation. Kindling acquisition varied with the intra-amygdala site of stimulation. During stimulation of the medial (AME) or central (ACE) nucleus, the only effect of estradiol replacement (E), compared to non-replaced rats (nE), was to significantly decrease the number of trials with afterdischarge (AD) during early kindling (stage 0). In rats receiving stimulation of the cortical nucleus (ACO) or the baso-lateral group of nuclei (ABL), a similar effect of estradiol was extended through stage 1. In addition, nE rats with ACO or ABL electrodes required significantly more trials with AD and accumulated more than twice the sec of AD during the late stages of kindling, compared to E rats and regressed to lower stage responses between the first stage 4 and last stage 5 responses; regressed responses never occurred in E rats. Estradiol also significantly decreased the prekindling AD threshold of the AME and ACE. These results indicate that estradiol accelerates early stage kindling, likely by proconvulsive properties to increase excitability within immediate amygdala projections. During late kindling stages, estradiol may participate in reinforcing or sustaining the convulsive readiness of kindling circuits established during bilateral recruitment. The site of action for this latter effect of estradiol may reside within circuits accessed by stimulation of the ACO or ABL, and not the AME or ACE.

Amygdala↗