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PubMed1987

The effects of ovariectomy and 17 beta-estradiol on cortical bone histomorphometry in growing rats.

The effects of ovariectomy for four weeks and of 17 beta-estradiol for three weeks on histomorphometry of the tibial diaphysis were determined in young rats. The effects of ovariectomy on histomorphometry of subcutaneous implants of demineralized bone matrix were also examined. Groups of young female rats were either ovariectomized or sham operated. After surgery, the animals were weight matched and pair fed. Despite the same caloric intake, ovariectomized rats grew more rapidly than pair-fed, sham-operated controls but were significantly heavier at sacrifice in only one of three experiments. Ovariectomy did not change mean serum calcium, phosphate, 25-hydroxyvitamin D (25-OHD), or 1,25-dihydroxyvitamin D [1,25(OH)2D] but significantly lowered mean serum magnesium. Serum estradiol was not detectable in ovariectomized animals. 17 beta-Estradiol in ovariectomized animals significantly increased mean serum estradiol and lowered mean serum phosphate but did not change mean serum calcium, magnesium, 25-OHD, or 1,25(OH)2D, as compared to values in sham-operated controls. Bone formation rate was significantly enhanced in ovariectomized animals at both the endosteal and periosteal surfaces of the tibial diaphysis as compared to values in sham-operated controls. The increase in bone formation rate was reversed by 17 beta-estradiol at the periosteal but not endosteal surface. Ovariectomy increased the bone apposition rate, mineralization rate, and osteoid thickness of the tibial diaphysis. These increases were reversed by 17 beta-estradiol. In implants, ovariectomy increased the resorption of implant matrix and enhanced the formation of new matrix. Ovariectomy resulted in increases in forming surface and resorbing surface in the implants.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2001

Localization of estradiol-responsive region in the phenobarbital-responsive enhancer module of mouse Cyp2b-10 gene.

The mouse Cyp2b-10 gene is inducible by treatment with estradiol as well as so-called phenobarbital (PB)-like inducers. To identify 5'-flanking elements responsible for induction by estradiol, we carried out reporter gene assays using a primary mouse hepatocyte culture system. Cyp2b-10 gene-driven luciferase activities were induced by estradiol as well as PB in this system. Deletion analysis demonstrated that the sequence contained within the region from -2331 bp to -2281 bp was responsible for the estradiol-induced luciferase activity. This region corresponds to the core element of PB-responsive enhancer module (PBREM). Several nucleotide mutations in the putative binding sites of the PBREM core element showed that the NR1 site was required for estradiol induction, and the same element was required for PB induction. These results indicate that estradiol induces Cyp2b-10 gene expression via PBREM.

Animals↗

PubMed2004

17beta-estradiol downregulates beta3-integrin expression in differentiating and mature human osteoclasts.

The increased bone resorption observed after estrogen withdrawal is responsible for bone loss and may lead to osteoporosis. The mechanism by which estradiol inhibits bone resorption is known to involve decreased osteoclastogenesis, however, the effect on osteoclast adhesion remains unclear. We examined the in vitro effect of estradiol and raloxifene on human osteoclast differentiation and function. Human peripheral blood mononuclear cells were cultured with M-CSF/RANK-L for 18 days, and we evaluated bone resorption, the expression of the protein and mRNA of the integrins, c-jun and c-fos in the presence or absence of estradiol. In this human model, beta3-integrin expression increased at the mRNA and protein levels during osteoclast differentiation, whereas that of beta5-integrin did not. We found that estradiol and raloxifene directly inhibited bone resorption on bone slices by 50%, and decreased the expression of beta3-integrin mRNA (60%) and protein (20%) in a time-dependent manner. Moreover, the mRNAs of c-fos and c-jun were both diminished by estradiol and raloxifene, particularly in early osteoclasts, but also to a lesser extent in mature cells. These findings suggest that the direct inhibitory action of estradiol on bone resorption may affect human osteoclast differentiation through downregulation of c-fos and c-jun and adhesion through modulation of beta3-integrin.

Blotting, Western↗

PubMed2001

beta-estradiol stimulation of DNA synthesis requires different PKC isoforms in HepG2 and MCF7 cells.

The role exerted by protein kinase C (PKC) on estrogen-induced DNA synthesis has been investigated in hepatic and mammary gland cells, HepG2 and MCF7. 17-beta-estradiol stimulated DNA synthesis in HepG2 and MCF7 cells, maximal effect occurring at 10 nM. DNA synthesis stimulation was prevented by anti-estrogen ICI 182,780 and by inhibitor of PKC, Ro 31-8220. The rapid estradiol effects in MCF7 cells were determined by following the inositol trisphosphate (IP(3)) production and PKC-alpha membrane translocation. After estradiol treatment the increase of IP(3) production, prevented by anti-estrogen or by phospholipase C (PLC) inhibitor (neomycin), was present in MCF7 cells. In MDA cells, devoid of estrogen receptor, no effect was observed. The PKC-alpha presence on the membranes appeared unchanged in MCF7 cells. The PLC inhibitors, neomycin and U73,122, and PKC-alpha down regulator, phorbol 12-myristate 13-acetate (PMA), were able to prevent estradiol-induced DNA synthesis in hepatoma cells, but ineffective in mammary cells; wortmannin, an inhibitor of phosphoinositide 3-kinases (PI3-K), blocked DNA synthesis in both cell lines. These data show that beta-estradiol, via an estrogen receptor-mediated mechanism, activates more signal transduction pathways, and consequently different PKC isoforms in two responsive cell lines. In both cell lines PI3-K/PKC pathway is functional to the estrogen regulation of DNA synthesis, whereas in HepG2 cells the parallel involvement of the PLC/PKC-alpha pathway is present. The reported results indicate that the DNA synthesis stimulation by beta-estradiol requires the estrogen receptor and utilises one or more activated pathways in dependence on the cell equipment.

Androstadienes↗

PubMed1982

In the absence of protein, estradiol suppresses meiosis of porcine oocytes in vitro.

The effect of estradiol on the spontaneous maturation of porcine oocytes was investigated. Cumulus-enclosed (intact) and cumulus-free (denuded) oocytes were cultured in the presence of estradiol-17 beta (0 to 10 microgram/ml) in a chemically defined bicarbonate-buffered medium that contained either dextran or BSA, or in a complex Hepes-buffered medium that was supplemented with serum. After 24 hr, chromatin spreads were prepared and meiotic maturation was scored. The biochemical integrities of the cumulus cells were assessed by determination of the estradiol and progesterone content of spent media after culture of intact oocytes in the presence of 0.5 X 10(-6) M testosterone and 10 microgram/ml follicle-stimulating hormone. Estradiol did not significantly affect the onset of maturation of either intact or denuded oocytes that were cultured in medium containing either BSA or serum. In serum-supplemented medium, however, the progression of maturation beyond metaphase I was significantly affected by the steroid in a dose-dependent manner. The steroid significantly inhibited the release from meiotic arrest of both types of oocyte cultured in medium supplemented with dextran. Supplementation of all media with testosterone and FSH significantly stimulated the synthesis of estradiol by the cumulus cells, compared with that of control groups. The synthesis of progesterone, however, was significantly stimulated by testosterone and FSH only in the BSA and serum-supplemented media. It is concluded that exogenous estradiol has the capacity to arrest meiosis in vitro but that this capacity can only be expressed if no exogenous protein(s) is present. In the absence of exogenous protein, progesterone synthesis by the adherent cumulus cells is minimal.

Animals↗

PubMed1994

Effect of exogenous estradiol applied at different embryonic stages on sex determination, growth, and mortality in the leopard gecko (Eublepharis macularius).

Temperature-dependent sex determination (TSD) occurs in three orders of reptiles. Several studies have examined the ability of estradiol to produce female hatchlings incubated at a male-producing temperature. The results of these experiments support the idea that estradiol could be used as a powerful tool in the conservation of endangered species with TSD by manipulating hatchling sex ratios. However, these experiments have concentrated on the mechanism of determination. This experiment was designed to test the efficacy of various dosages of estradiol applied at two different stages to alter the hatchling sex ratio as well as determining the potential use of such manipulation for conservation efforts by monitoring egg mortality and hatchling growth. The leopard gecko (Eublepharis macularius) exhibits TSD and reaches reproductive maturity in less than one year, making it an excellent model for evaluating the long-term effects of estradiol. The results demonstrate that estradiol has a dose-dependent effect on the hatchling sex ratio while only high dosages applied at the later stage of development showed increased mortality. Estrogen-determined females grew at the same rate as temperature-determined females and have produced viable hatchlings. Estradiol treatment of eggs from endangered species may provide a method of insuring female offspring when the TSD pattern is unknown or equipment for controlled incubation is unavailable.

Animals↗

PubMed2002

Neuroprotective effect of estradiol and phytoestrogens on MPP+-induced cytotoxicity in neuronal PC12 cells.

A large body of experimental evidence supports a role for oxidative stress as a mediator of nerve cell death in Parkinson's disease. To better understand the cellular insult of oxidative stress on dopaminergic neurons, we studied the cytotoxic effect of the 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) metabolite, 1-methyl-4-phenyl pyridium (MPP(+)), on several parameters of cell distress using neuronal PC12 cells. We also measured the level of protein expression for the dopamine transporter and the estrogen receptors alpha and beta. Since estrogens have been reported to prevent neuronal degeneration caused by increased oxidative burden, we investigated the ability of 17beta-estradiol, the stereoisomer 17alpha-estradiol, and several phytoestrogens to rescue neuronal PC12 cells submitted to MPP(+)-induced cytotoxicity. Our results consistently show a protective effect of 17alpha-estradiol, 17beta-estradiol and certain phytoestrogens such as quercetin and resveratrol, in neuronal PC12 cells treated with MPP(+). In our cellular paradigm, phytoestrogens coumestrol, genistein, and kaempferol did not revert MPP(+)-induced cellular death. By Western blot, we demonstrated that administration of MPP(+) alone decrease dopamine transporter expression, while treatments with MPP(+) together with 17alpha-estradiol, 17beta-estradiol, quercetin, or resveratrol could restore dopamine transporter protein expression to control levels. Moreover, the same treatments did not modulate alpha estrogen receptor or beta estrogen receptor expression. By these studies, we aim to provide more evidence for the involvement of phytoestrogens in the process of neuroprotection and to test our hypothesis that some of these compounds may act as neuroprotective molecules and have a lesser hormonal effect than estrogens.

1-Methyl-4-phenylpyridinium↗

PubMed1988

Antiestrogens do not counteract the inhibitory effect of estradiol-17 beta on the growth of the Dunning R3327 prostatic adenocarcinoma.

The purpose of this study was to investigate if the local effects of estradiol on the Dunning R3327 prostatic adenocarcinoma were estrogen-receptor mediated. All rats with the transplantable Dunning R3327 prostatic adenocarcinoma were castrated on the first day of treatment and were supplemented with daily s.c. injections of testosterone propionate (0.1 mg) during the treatment period, lasting for 6 weeks. The following treatment groups were studied: castration + testosterone supplementation (C + T, control group), C + T and estradiol-17 beta (50 micrograms/daily s.c.), C + T and tamoxifen (1 mg twice a week s.c.), and C + T and estradiol-17 beta in combination with tamoxifen. Tumor volumes were measured every week. At the end of the treatment period, pieces of the tumors were taken for morphological studies and estrogen-receptor analysis. In the groups of rats given tamoxifen treatment no estrogen-receptor binding was detectable in prostatic tumors, but, despite this, tamoxifen did not prevent either the inhibitory effect of estradiol-17 beta on the tumor growth rate or the estrogen-induced decrease of volume density of prostatic glandular epithelium. In contrast, the estrogen-induced increase of volume density of the stroma was abolished by tamoxifen, suggesting that this effect may be mediated by the estrogen receptor. A morphometrical method for estimating the growth of different tumor compartments is presented. Treatment with estradiol-17 beta, both with or without combined treatment with tamoxifen, reduced the growth of both the tumor epithelium and stroma. The direct effect of estradiol-17 beta on the growth and morphology of the Dunning R3327 prostatic adenocarcinoma seemed not to be mediated by the estrogen receptor.

Adenocarcinoma↗

PubMed1981

Effect of ethinyl estradiol on development of mouse fetuses.

Pregnant ICR/JCL mice were given orally 0.02, 0.3, or 2.0 mg/kg body weight/day of ethinyl estradiol in olive oil or vehicle alone on day 11 through day 17 of pregnancy. Pregnant mice of another group received a single oral dose of ethinyl estradiol on day 8 or day 11 of pregnancy. A lethal effect on fetuses of both groups with single and continuous exposure to ethinyl estradiol was observed in a dose-response relationship. Growth suppression of fetuses was only found at term in a dose-response relationship following continuous exposure to ethinyl estradiol. Hypertrophic nipples were seen in 42% of surviving female fetuses prenatally exposed to 2.0 mg/kg of ethinyl estradiol singly on day 11 of gestation. There was not an increase in other congenital malformations in any of the treated groups. These findings indicate that administered ethinyl estradiol can affect the developing mouse embryo but the embryotoxic doses in the mouse are substantially greater than the usual therapeutic or contraceptive doses in the human.

Abnormalities, Drug-Induced↗

PubMed2001

Role of ERK1/2 in the differential synthesis of progesterone and estradiol by granulosa cells.

A major concept in mammalian ovarian physiology is that follicle-stimulating hormone (FSH) activates the granulosa cells (GCs) in the Graafian follicle to selectively produce estradiol, but not progesterone, during the follicular phase of the menstrual or estrous cycle. However, given the fact that FSH can induce production of both estradiol and progesterone by GCs cultured in vitro, it has been postulated for a long time that there is a factor present in the ovary that selectively prevents FSH-induced progesterone production. Here, we provide evidence that two members of the mitogen-activated protein kinase family, extracellular signal-regulated kinase-1 and -2 (ERK1/2) can differentially regulate FSH-stimulated estradiol and progesterone production. Using primary rat GCs from early antral follicles cultured in serum-free medium for 48 h, we found that the addition of a specific inhibitor of ERK1/2 activation, U0126, caused the attenuation or enhancement of FSH-induced progesterone or estradiol production, respectively, in a dose-dependent manner. Throughout the 48-h culture period in this culture system ERK1/2 molecules in their activated state (phospho-ERK1/2) were clearly detectable in GCs exposed to FSH. The addition of U0126 caused a decrease in the levels of phosphorylated but not unphosphorylated ERK1/2 which was maintained throughout the 48-h culture, suggesting that U0126 was continuously active to inhibit the phosphorylation of ERK1/2. The divergent regulation of FSH-induced progesterone and estradiol synthesis by U0126 was further supported by demonstrating that U0126 inhibits and stimulates FSH-induced mRNA levels of steroidogenic acute regulatory protein and P450 aromatase, respectively. Collectively, this study clearly identified ERK1/2 as the first intracellular signaling molecules that differentially regulate FSH-induced progesterone and estradiol synthesis in GCs.

Animals↗

PubMed2001

Transforming growth factor-beta regulation of estradiol-induced prolactinomas.

Prolactin-secreting adenomas (prolactinomas) are the most prevalent form of pituitary tumors in humans, and increased tumor growth under estrogenic influence in female patients is often of clinical concern. Extensive experimental work has uncovered the roles of estrogen receptors and various growth-regulatory peptides in estradiol action on lactotropes. However, it is only recently that we are beginning to gain insight into how these growth factors interact to regulate estradiol action on lactotrope cell proliferation. Recent studies have identified the regulatory role of TGF-beta-related peptides in estradiol action on lactotropes. Additionally, these studies determined that TGF-beta and FGF interact to facilitate the communication between lactotropes and folliculostellate cells that is necessary for the mitogenic action of estradiol. This review addresses the role of estradiol in prolactinoma formation and summarizes data that support a novel concept: Alterations in the expression and action of TGF-beta isoforms are crucial steps in estradiol-induced tumorigenesis.

Animals↗

PubMed1995

The relative effectiveness of androstenedione, testosterone, and estrone, precursors to estradiol, in sex reversal in the red-eared slider (Trachemys scripta), a turtle with temperature-dependent sex determination.

Androstenedione↗

PubMed1996

The relative effectiveness of estrone, estradiol-17 beta, and estriol in sex reversal in the red-eared slider (Trachemys scripta), a turtle with temperature-dependent sex determination.

In many turtles the temperature during the middle of incubation determines the gonadal sex of the hatchling. Sex steroid hormones have been implicated in temperature-dependent sex determination in the red-eared slider turtle, Trachemys scripta; nonaromatizable androgens are involved in male sex determination and estrogens and aromatizable androgens in female sex determination. Administration of exogenous estradiol-17 beta to eggs incubating at a temperature that normally produces only males can overcome the effect of temperature and result in all offspring being female. Further, estradiol-17 beta and incubation temperature synergize to produce a greater feminizing effect at intermediate incubation temperatures that produce mixed sex ratios. This study demonstrates that, in the red-eared slider, there is a complex interaction between incubation temperature, different estrogens, and the dosage effect of each hormone. There are changes in potency of different estrogens with incubation temperature such that estriol is more potent than estrone and estradiol-17 beta at 26 degrees (an all-male producing incubation temperature), estrone and estriol are equipotent to each other and more potent than estradiol-17 beta at 28.8 degrees (an incubation temperature that produced a male-biased sex ratio), and estradiol-17 beta is more potent than estrone and estriol at 29 degrees (an incubation temperature that produced equal numbers of males and females). These changes may be due to differences in synergism between the hormones and incubation temperature. Estriol treatment also resulted in cranially hypertrophied oviducts at all incubation temperatures in a dose-dependent manner, whereas animals treated with estradiol-17 beta and estrone had normal oviducts. These results support the hypothesis that estrogens are involved in the final common pathway of female sex determination in this species.

Animals↗

PubMed1999

Enhancement of post-ischemic myocardial function by chronic 17 beta -estradiol treatment: role of alterations in glucose metabolism.

This study was designed to assess the effects of chronic estrogen replacement therapy on mechanical function and glucose utilization in aerobic and post-ischemic hearts. Ovariectomized female rats were either untreated or were treated subcutaneously with 17 beta -estradiol (0.25 mg 21-day slow release pellets). After 14 days, when serum concentrations of 17 beta -estradiol were 3.8+/-0.8 and 148+/-15 pg/ml, respectively, hearts were isolated and perfused in working mode with Krebs-Henseleit solution containing 1.2 m m palmitate and 11 m m[5-(3)H/U-(14)C]glucose. Hearts were perfused aerobically (60 min) and then subjected to low-flow ischemia (0.5 ml/min, 60 min) followed by reperfusion (30 min). During reperfusion, hearts from rats treated chronically with 17 beta -estradiol had an improved (two-fold) recovery of mechanical function. 17 beta -estradiol (400 p m, 109 pg/ml), when present acutely in heart perfusate during ischemia and reperfusion, did not improve recovery. Chronic 17 beta -estradiol increased glucose oxidation during reperfusion as well as during aerobic perfusion but had no effect on glycolysis. Chronic 17 beta -estradiol also altered post-ischemic glycogen metabolism and increased glycogen content and glycogen synthase activity at the end of reperfusion. As stimulation of glucose oxidation has been shown previously to be cardioprotective, and as the enhanced rate of glucose oxidation was not simply a consequence of enhanced recovery of mechanical function, alterations in glycogen and glucose utilization may contribute to the direct cardioprotective effects of chronic estrogen treatment.

Animals↗

PubMed1994

Somatostatin mRNA levels within the periventricular nucleus are regulated by estradiol and insulin-like growth factor-I in immature female rats.

Adolescent growth is regulated by developmental increases in growth hormone (GH) secretion. Although the hypothalamic release of GH-releasing hormone (GHRH) stimulates and the release of SRIF inhibits GH secretion, it is not known how these regulatory mechanisms change developmentally. In addition, GH secretion is facilitated during maturation by increases in peripheral estradiol and may be inhibited, via a negative feedback mechanism, by insulin-like growth factor-I (IGF-I). It is not clear whether these act through the hypothalamic regulation of GHRH and somatostatin (SRIF). In order to further understand the regulation of GH secretion during development, the present study determined how estradiol and IGF-I altered SRIF mRNA in the hypothalamus in immature female rats. The working hypotheses were that estradiol would decrease SRIF mRNA accounting, in part, for its positive effect on GH release and IGF-I would increase SRIF mRNA representing a negative feedback mechanism regulating GH secretion. Preprosomatostatin (ppSRIF) mRNA levels within the periventricular nucleus (PeVN) were measured with in situ hybridization in ovariectomized female rat pups (n = 5 per group). Infusions were delivered sc via either a Silastic capsule (oil, 10 or 60 micrograms/ml estradiol) or an osmotic minipump (acetic acid, 120 or 240 micrograms IGF-I/day). Following ovariectomy on Day 21, animals were treated for either 1 or 7 days beginning on Day 24 of age. A total of 18 treatment groups were evaluated, including control, estradiol alone, IGF-I alone, and estradiol and IGF-I combined at both doses and treatment durations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2001

Mono-(2-ethylhexyl) phthalate suppresses aromatase transcript levels and estradiol production in cultured rat granulosa cells.

The female reproductive toxicity of di-(2-ethylhexyl) phthalate and its active metabolite mono-(2-ethylhexyl) phthalate (MEHP) is attributed to suppression of ovarian granulosa cell estradiol production. In these studies, several structurally related phthalates (0-200 microM) and Wy-14,643 (0-100 microM) were compared to MEHP for their effects on granulosa cell estradiol production and transcript levels of cytochrome P450 enzyme CYP 19, also known as aromatase (P450arom), the rate-limiting enzyme in the conversion of androgens to estrogens. Granulosa cells were obtained from 28-day-old Fisher 344 rats and were cultured for 48 h. Test chemical or DMSO was added at the time of culture, along with testosterone as a substrate for aromatase. 17beta-Estradiol production was measured by standard radioimmunoassay, mRNA was measured by fluorescent RT-PCR, and protein was measured by Western blot analysis. MEHP was unique among the phthalates in its ability to decrease estradiol production, while Wy-14,643 had effects similar to MEHP at 100 microM. MEHP and Wy-14,643 also significantly decreased aromatase mRNA levels. The decrease in mRNA was concentration dependent and was paralleled by a decrease in aromatase protein. MEHP did not alter levels of CYP 11A1, the cholesterol side-chain cleavage enzyme (P450scc). Treatment with a cAMP analogue increased expression of P450scc in the presence of MEHP (100 to 200 microM) while the decrease in aromatase remained. Thus, these studies suggest that MEHP is distinct from several structurally related phthalates but similar to the peroxisome proliferator Wy-14,643 in its action on granulosa cell estradiol production. Moreover, the suppression of estradiol by MEHP is likely mediated through its action on aromatase transcript levels independent of cAMP-stimulated regulation.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed2001

Regulation of 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced tumor promotion by 17 beta-estradiol in female Sprague--Dawley rats.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a potent hepatocarcinogen in female but not in male rats. In an initiation-promotion model, ovariectomy inhibits TCDD-induced cell replication and reduces both TCDD-induced tumor formation and the promotion of enzyme-altered hepatocellular foci (AHF). The aim of this study was to determine the involvement of the ovarian hormone 17 beta-estradiol in the induction of cell proliferation and development of putative preneoplastic AHF following chronic exposure to TCDD. Diethylnitrosamine (DEN)-initiated ovariectomized (OVX) female rats were treated with TCDD for 20 or 30 weeks in the presence and absence of 17 beta-estradiol administered continuously by implanted 90-day release pellets. Following 20 weeks of treatment, cell proliferation in TCDD-treated rats was decreased regardless of ovarian hormones. Following 30 weeks of exposureTCDD, only significantly induced cell proliferation in OVX rats receiving supplemental 17 beta-estradiol. These data demonstrate that the the transitory mitoinhibition of cell replication by TCDD is not hormonally responsive, but that induction of cell replication at later time points is. TCDD exposure resulted in elevated AHF expressing gamma-glutamyltranspeptidase (GGT) in intact, but not OVX rats at both time points. TCDD also induced GGT-positive AHF in 17 beta-estradiol-supplemented OVX rats. TCDD induced AHF expressing the placental form of glutathione-S-transferase (PGST) in both intact and OVX rats regardless of 17 beta-estradiol exposure, indicating that the modulating effect of 17 beta-estradiol on AHF was specific to the GGT-positive phenotype.

Animals↗

PubMed1990

Effect of 17 beta-estradiol on calcium response to phytohaemagglutinin in human lymphocytes.

Pre-treatment of human lymphocytes with 17 beta-estradiol diminishes the increase in concentration of cytosolic free calcium after stimulation with phytohaemagglutinin. The effect is dependent on 17 beta-estradiol concentration and on the preincubation time. The effect is not due to an interaction between 17 beta-estradiol and phytohaemagglutinin, but appears to be a consequence of the binding of the hormone to the cell surface. The effect is specific for 17 beta-estradiol, since the alpha isomer and other steroid hormones (progesterone, testosterone, diethylstilbestrol and 5 alpha-androstan) have no effect. Since the effect of the 17 beta-estradiol can be suppressed by treatment of lymphocytes with ouabain, it appears that the effect of estradiol on the rise of cytosolic calcium induced by phytohaemagglutinin is mediated by the (Na, K)-ATPase.

Calcium↗