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PubMed2000

Differential effects of 17beta-estradiol and testosterone on the contractile responses of porcine coronary arteries.

1. We investigated the effects of short-term exposure to physiological levels of 17beta-estradiol and testosterone on vasocontractile responses in porcine coronary artery rings. 2. Concentration-response curves to endothelin-1, 5-hydroxytryptamine, the thromboxane analogue U46619 and KCl were constructed in endothelium-intact and endothelium-disrupted artery rings. 3. Thirty minutes exposure to 17beta-estradiol (1 and 30 nM) significantly attenuated vasoconstriction to endothelin-1, 5-hydroxytryptamine and U46619. Conversely, the same concentrations of testosterone significantly potentiated responses elicited by these contractile agents. These inhibitory effects of 17beta-estradiol and enhancing actions of testosterone on contractions were endothelium-independent. KCl-mediated contractions were unaffected by the presence of either sex hormones. 4. The oestrogen receptor antagonists, tamoxifen (10 microM) and ICI 182,780 (10 microM), were unable to reverse the inhibitory influence 1 nM 17beta-estradiol had on the agonist-mediated contractile responses. Similarly, the androgen receptor antagonists, flutamide (10 microM) and cyproterone acetate (10 microM), failed to affect the potentiating activities of 1 nM testosterone. The alteration in vasoconstrictive responses observed following acute exposure to either 1 nM 17beta-estradiol and 1 nM testosterone were apparent even in the presence of the protein synthesis inhibitor cycloheximide (10 microM) and the transcription inhibitor actinomycin D (10 microM). 6. In conclusion, we report a unique type of sex hormone action on the coronary vasculature. These events occur at low nanomolar concentrations of 17beta-estradiol and testosterone, are insensitive to conventional sex hormone receptor antagonists, are not blocked by de novo protein synthesis inhibitors and have rapid time-courses that are uncharacteristic of classical genomic activities.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2006

Estradiol alters only GAD67 mRNA levels in ischemic rat brain with no consequent effects on GABA.

The present study tested the hypothesis that estradiol reduces tissue infarction after middle cerebral artery occlusion (MCAO) in estradiol-deficient females by augmenting glutamic acid decarboxylase (GAD) expression and thus activity, leading to increases in gamma-amino-butyric acid (GABA) tissue levels. Glutamic acid decarboxylase is the principal enzyme for GABA synthesis and has two isoforms, GAD65 and GAD67, which differ in size and cellular distribution. Rats were ovariectomized 7 to 8 days before receiving no hormone, placebo, or 25 microg estradiol via subcutaneous implant 7 to 10 days before harvesting tissue in either ischemic cohorts after 2 h of MCAO (end-ischemia) or in nonischemic cohorts. Selected cortical and striatal regions were microdissected from harvested brains. GAD65/67 mRNA levels were determined by microlysate ribonuclease protection assay. End-ischemic GABA concentrations were determined by HPLC. Steroid treatment selectively decreased ischemic cortical GAD67 mRNA levels. In most brain regions evaluated, regional GABA concentrations increased with ischemia regardless of treatment. Estradiol blocked MCAO-induced increases in GABA concentration only in dorsomedial cortex. These data suggest that estradiol repletion in ischemic rat brain selectively decreases GAD67 mRNA levels but does not alter steady-state GABA concentrations. It may be that estradiol under ischemic conditions is attenuating GABA metabolism rather than enhancing synthesis or is augmenting other aspects of GABAergic transmission such as GABA transporters and receptors.

Animals↗
PubMed2002

Upregulation of estrogen and androgen receptors modulate expression of FGF-2 and FGF-7 in human, cultured, prostatic stromal cells exposed to high concentrations of estradiol.

This study was performed to develop an experimental model in which expression of estrogen receptors (ER) by human prostatic stromal cells could be reproducibly enhanced relative to similar cells with low ER expression. The second aim was to characterise changes in expression of ER, androgen receptor (AR), FGF-2 and FGF-7 in stromal cells exposed to high and low concentrations of estradiol and testosterone mimicking the different sex hormone levels between young and elderly men. Five strains of human prostatic stromal cells, isolated from BPH resections, were grown in steroid-free medium plus 1 micromol 17beta-estradiol. After 10 days, cells were passaged and grown in the same medium without estradiol until confluent. In a second study four cell strains were exposed to high and low concentrations of 17beta-estradiol and testosterone for 10 days. Cells were labelled with fluorescent antibodies to ERalpha, AR, FGF-2 and FGF-7 and the fluorescence intensity measured by flow cytometry. Following exposure to 1 micromol estradiol, stromal cells showed reduced expression of AR and ERalpha but after passage without estradiol they showed a 25% increase in both receptors over controls. Different combinations of sex hormones induced inconsistent changes with respect to expression of ER, AR and FGFs in the various cell-strains. However, there was a highly significant correlation between AR, ER and FGF-2 and FGF-7, which was cell strain-specific. Thus, changes in sex hormone balance per se may not be solely responsible for the observed increases in prostatic ER levels in BPH. Since expression of ER is correlated with synthesis of FGF-2 and FGF-7, it is likely that increases in stromal ER may mediate the synthesis of stromally-derived growth factors which contribute to the aetiopathogenesis of benign prostatic hyperplasia.

Culture Techniques↗
PubMed1998

T lymphocytes are not the target for estradiol-mediated suppression of DTH in reconstituted female severe combined immunodeficient (SCID) mice.

Oestrogen has the capacity to suppress T cell-dependent DTH. To explore the mechanisms whereby oestrogen exerts its effects on the immune system we have used SCID mice which are largely devoid of functional T and B lymphocytes, hence being unable to raise DTH, but display intact antigen-presenting capacity. Transfer of lymphocytes to SCID mice restores the DTH capacity. In order to analyse if oestrogen down-regulates DTH by a direct action on T cells we reconstituted SCID mice with either splenocytes or thymocytes from congenic C.B-17 or allogeneic B6 donor mice. Either donor or recipient mice were exposed to estradiol before cell transfer. DTH response was registered in recipient SCID mice 1 and 3 weeks after challenge with oxazolone (OXA). SCID mice receiving estradiol-exposed spleen cells from congenic or allogeneic donor mice displayed lower DTH responses compared with control mice. In contrast, SCID mice receiving estradiol-exposed thymocytes from congenic donor mice showed no significant difference in DTH response compared with control mice. Estradiol-treated SCID mice, transferred with either spleen cells or thymocytes from congenic, hormonally non-treated donors, displayed a significantly lower DTH response compared with control mice. In contrast, estradiol-treated SCID mice receiving hormonally non-treated allogeneic spleen cells showed no difference in DTH response compared with control mice. The results show that T lymphocytes are not the target cell population for estradiol-mediated suppression of DTH in reconstituted female SCID mice.

Adjuvants, Immunologic↗
PubMed1996

Estradiol regulation of alpha 1b-adrenoceptor mRNA in female rat hypothalamus-preoptic area.

Estradiol treatment for 48 h increases the density of alpha 1B-adrenoceptors in the hypothalamus-preoptic area of ovariectomized female rats by five- to six-fold. Present studies tested the hypothesis that estradiol elevation of hypothalamus-preoptic area alpha 1B-adrenoceptor density is correlated with increased levels of mRNA for this receptor. We developed a semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) protocol for measuring brain alpha 1b-adrenoceptor mRNA. The primers chosen yielded the predicted 409 base pair PCR product when used to amplify authentic alpha 1b-adrenoceptor cDNA. The identity of the RT-PCR products from rat brain was confirmed by restriction digest analysis and sequencing. Moreover, there was a good correlation between the levels of alpha 1b-adrenoceptor mRNA measured by RT-PCR in liver, whole brain and cerebellum with previous measurements using Northern blots and RNAse protection assays. We then performed RT-PCR on total RNA from hypothalamic-preoptic area tissue taken from ovariectomized control rats and from ovariectomized rats injected once or twice with 2 micrograms of estradiol benzoate at 24 or 24 and 48 h before sacrifice. Exposure to estradiol for either 24 or 48 h significantly increased levels of alpha 1b-adrenoceptor mRNA by 86-110% in the hypothalamus-preoptic area of ovariectomized female rats when compared to oil-treated controls. We also examined whether estradiol regulates alpha 1b-adrenoceptor mRNA in the cortex. Cortical alpha 1b-adrenoceptor mRNA levels were reduced to approximately 20% of control levels when measured 24 h after hormone injection. A similar decrease in cortical alpha 1b-adrenoceptor mRNA was observed 48 h after estrogen administration. In summary, estradiol treatment significantly increases the level of alpha 1b-adrenoceptor mRNA in the hypothalamus-preoptic area, a brain region involved in the control of reproductive function. In the cortex, a brain region with relatively few estrogen receptors, the same estrogen treatment reduces alpha 1b-adrenoceptor mRNA levels.

Animals↗
PubMed2001

Anti-inflammatory effects of 17beta-estradiol pretreatment in men after coronary artery surgery.

OBJECTIVE: To investigate the anti-inflammatory and hemodynamic effects of 17beta-estradiol in men undergoing elective coronary artery bypass graft surgery (CABG). DESIGN: Prospective, randomized, controlled. SETTING: Operating room and intensive care unit in a university hospital. PARTICIPANTS: Twenty-one men undergoing primary, elective CABG surgery. INTERVENTION: 17beta-estradiol, 2mg, was given orally twice in 14 hours before the operation. MEASUREMENTS AND MAIN RESULTS: Leukocyte counts, plasma myeloperoxidase, tumor necrosis factor-alpha, interleukin (IL)-6, IL-8, and IL-10 were measured perioperatively. Leukocyte counts were lower in the 17beta-estradiol group than in controls at 6 hours (11.4 +/- 2.0 hours v 15.5 +/- 4.7 hours x 10(9)/L) and 20 hours (11.6 +/- 1.9 hours v 13.6 +/- 2.5 hours x 10(9)/L) after reperfusion (p = 0.03). The release of myeloperoxidase was lower in the 17beta-estradiol group than in controls (5 minutes; 634.4 +/- 213.1 microg/mL v 773.1 +/- 209.3 microg/mL; 4 hours, 305.0 +/- 108.0 microg/mL v 441.3 +/- 191.6 microg/mL; p = 0.02). Systemic vascular resistance index was lower just after cardiopulmonary bypass, and cardiac index was higher postoperatively in the 17beta-estradiol group as compared with controls. CONCLUSION: Pretreatment with 17beta-estradiol can limit leukocyte activation in men after CABG surgery.

Administration, Oral↗
PubMed1978

Estradiol and progesterone binding in rabbit placenta during gestation.

In rabbit fetal placenta, 17 beta-estradiol and progesterone are not bound by specific (high affinity, low capacity) components in the cytosol, in spite of the fact that this part of the organ is very reactive to modifications in hormonal conditions. Cytosol receptors for estradiol and progesterone are found only in the maternal part of the placenta; apparent association constants are about 3 X 10(8) M-1 for 17 beta-estradiol and about 2 X 10(8) M-1 for progesterone (in the absence of glycerol) at 4 degrees C. Estradiol is also bound to nuclei in cells of the maternal placenta in vivo and in vitro. Concentrations of estradiol and progesterone binding sites show marked variations during normal gestation in the rabbit. For estradiol the number of binding sites increases from day 10 to day 14, then decreases until parturition. This number increases for progesterone from day 10 to day 16, then decreases until day 27.

Animals↗
PubMed1983

Biochemical cascade mediating the estradiol action.

The data suggest that estradiol enhances the formation of histamine in rat uterus by induction of histidine decarboxylase; histamine activates adenylate cyclase providing accumulation of cyclic 3',5'-AMP, which, probably, induces glycolytic enzymes via phosphorylation of chromatin proteins, and mediates other estradiol effects. The chain of successively acting enzymes and mediators constitutes, obviously, a cascade amplifying the estradiol action. Since histamine is known to act as an intercellular mediator, attempts were made to find out the distribution of estradiol, histamine, and cyclic 3',5'-AMP among uterine cells. Autoradiography has shown that 3H-estradiol is bound by the nuclei of myometrium cells, 3H-histamine was found in the cytoplasm of these cells, 3H-cyclic 3',5'-AMP is selectively bound by the cells of capillary endothelium of the uterus. The estradiol mediators seem to spread their effect on different types of cells which form together a kind of a multicellular functional system.

Adenylyl Cyclases↗
PubMed1993

Feeding status-related effects of 17 beta-estradiol on liver 3-hydroxy-3-methylglutaryl CoA reductase.

Total and expressed 3-hydroxy-3-methylglutaryl CoA reductase was determined in hepatic microsomes prepared from fasted and fed control rats and 17 beta-estradiol-treated rats. Plasma, liver and microsome cholesterol levels were also measured. Fasting resulted in significantly lower total and expressed specific activity of HMG-CoA reductase such that the expressed/total activity ratio doubled regardless of the endocrine status of the animals. Rats treated for either 3 or 21 days with 50 micrograms 17 beta-estradiol and starved for 24 hours exhibited greater reductase activity than untreated animals, the percentage of enzyme in effective form being maintained. When rats were fed on a commercial diet or a 4% cholestyramine-diet for five days, thus presenting higher basal HMG-CoA reductase levels, the stimulatory effect of 17 beta-estradiol was not statistically significant. In contrast, when total reductase was reduced by dietary cholesterol, the estrogen effect was accentuated. Long-term estradiol treatment was associated with increases in liver weight, decreases in free and total plasma cholesterol, and microsome cholesteryl ester accumulation; while short-term estradiol treatment increased plasma esterified and total cholesterol as well as the microsomal content of cholesteryl esters. These findings suggest (i) that the two 17 beta-estradiol treatments employed in this study are associated with higher HMG-CoA reductase levels and this is particularly apparent when cholesterol synthesis occurs at a low rate and (ii) that plasma cholesterol levels are not strictly correlated with hepatic HMG-CoA reductase activity.

Animals↗
PubMed1999

Efficacy on climacteric symptoms of a new estradiol transdermal patch with active matrix in comparison with a reference reservoir patch. Two long-term randomized multicenter parallel-group studies.

METHODS: Two randomized prospective multicentre parallel group studies were performed (one in Germany and the other in Italy) in symptomatic postmenopausal women. The goal was to assess the efficacy on climacteric symptoms and the safety of a new estradiol (CAS 50-28-2) transdermal patch with solid active matrix (SAM) in comparison to a conventional liquid reservoir (LR) type estradiol transdermal patch. Both patches released 50 micrograms/day estradiol. One group of patients received the SAM patch and the other the LR patch in 4-week cycles, with a twice-weekly application of the patches for 3 weeks, followed by one week without patches. Progestin opposition was achieved with medroxyprogesterone acetate 5 mg/day orally in the last 11 days of patch application in the German study and with 10 mg/day in the last 12 days of patch application in the Italian study. Both studies were divided into two Parts: Part 1 with three 4-week cycles for a total of 12 weeks and Part 2 for other ten 4-weeks cycles in which the patches could be applied also continuously. The total duration of the study was therefore 52 weeks. RESULTS: Germany study. 133 patients resulted randomized to the SAM group and 129 to the LR group. Both estradiol patches quickly relieved climacteric symptoms already during the first 3 weeks of patch application, as shown by the rapid decrease of the Kupperman Index. At the end of Part 1, in the SAM group 91% and in the LR group 96% of patients reported relief from climacteric symptoms. At the end of Part 2 the percentages were 98% and 95%, respectively. The two patches were therapeutically equivalent with a power greater than 99.7%. Both patches were systemically fairly well tolerated. Only 4.5% of patients in the SAM group and 3.9% in the LR group discontinued prematurely for possible adverse reactions related to estradiol. There was no significant difference between the two patches with regard to systemic tolerability. Conversely, with regard to local skin reactions, the SAM patch was significantly (p < 0.01) better tolerated than the LR patch. The adhesion to the skin of the SAM patches was better than that of the LR patches. RESULTS. Italian study. 139 patients resulted randomized to the SAM patch and 128 to the LR patch. Also in this study both types of patches relieved the climacteric symptoms already during the first 3 weeks of patch application, as shown by the rapid decrease of the visual analogue scale (VAS) recordings of severity of hot flushes and of sweats. At the end of Part 1 both patches relieved 95% of patients from climacteric symptoms. At the end of Part 2, i.e. after 52 weeks, 100% of patients were relieved from climacteric symptoms. Of these, 72% in the SAM group and 78% in the LR group reported complete disappearance of symptoms. Also in the Italian study, therefore, the two patches were found therapeutically equivalent. Both patches stopped or even reversed bone mineral loss in L2-L4 and had some favorable effects on lipid metabolism. Both patches were systemically equally fairly well tolerated with premature discontinuations for systemic adverse drug reactions in only 5.0% of patients in the SAM group and 3.9% in the LR group. Conversely, as in the German study, the SAM patches were significantly better tolerated by the skin (p < 0.0001). CONCLUSIONS: The two types of estradiol transdermal patches were equivalent in providing an effective and rapid relief from climacteric symptoms. Systemically both patches were fairly well tolerated. The SAM patches were significantly better tolerated by the skin. The better local tolerability combined with better adhesion and cosmetic properties render the SAM patches very patient friendly and improve the compliance in the long term estrogen replacement therapy required to reduce osteoporosis and cardiovascular risks.

Adhesiveness↗
PubMed2001

Coadministration of melatonin and estradiol in rats: effects on oxidant status.

This study was designed to investigate the effects of melatonin and estradiol (E2) on lipid peroxidation and antioxidant defense enzymes in blood and liver tissue when administered in vivo. Wistar albino rats were divided into three experimental groups and treated with either estradiol (25 mg/kg bw, s.c.), melatonin (i. p.), or melatonin plus E2, whereas control animals had diluent injections only. Melatonin was given 10 mg/kg bw x 2 intraperitoneally 30 min before and 60 min after E2 treatment to the melatonin plus E2 group. Animals were sacrificed three hours after the estradiol injection, and their blood and liver tissues were prepared for biochemical analyses. Tissue malondialdehyde (MDA) levels and antioxidant enzyme activities--superoxide dismutase (SOD) and glutathione peroxidase (GPx)--were determined in the postmitochondrial fraction, and the results were compared. Estradiol injection caused significant increases in both MDA levels and GPx activity in liver. When melatonin was administered in combination with E2, the effect of estradiol on MDA levels was abolished. A significant decrement in SOD activity occurred in melatonin-treated animals. GPx activity in the blood of E2 plus melatonin-injected animals was significantly higher than those in control animals. Melatonin-treated animals exhibited relatively lower levels of SOD activity than those from the control and E2 plus melatonin groups. This indicates that estradiol could exert oxidant action resulting in an increment in tissue malondialdehyde levels. Enhanced activity of GPx in both liver and blood following melatonin injection may indicate the contribution of this neurohormone on the antioxidant defense.

Animals↗
PubMed2003

[Impact of the cellular estradiol response on the therapeutic inhibition of growth factor signaling].

Cellular response to estradiol stimuli ist mediated by different signal transduction cascades. In addition to classical mechanisms like the activation of estrogen response elements, there is increasing interest in the so-called non- nuclear actions of estrogens. It has been shown, that the estradiol-induced activation of cytoplasmic kinases is an important alternative mechanism of the cellular estradiol response. Consequently, the question has been raised, whether estradiol-induced activation of growth factor signaling would be able to interfere with the action of antitumoral substances directed against receptor-tyrosine kinase signal transduction. Recent data demonstrated, that estradiol is able to diminish the effects of antitumoral drugs targeting the HER2 receptor in vitro. Novel insights into the non-nuclear estradiol response and its impact on the efficacy of antitumoral drugs observed in endometrial tumor cells are reviewed.

Antineoplastic Agents↗
PubMed2003

[Estrogen-dependent neoplasia - what is the significance of estradiol metabolites].

Estradiol can be metabolized to substances eliciting different, partly opposite effects even at low concentrations as shown in own investigations, e. g., regarding (anti)angiogenic actions. Specific anticancerogenic effects are ascribed to 2-hydroxyestrone and particularly 2-methoxyestradiol. In contrast, 16alpha-hydroxyestrone and the 4-hydroxyestrogens may be genotoxic under certain circumstances. Furthermore there are indications that endogenous production of proliferation-stimulating metabolites is raised in some cancers. Especially the urinary excretion of 2-hydroxyestrone to 16alpha-hydroxyestrone was investigated showing in own and other clinical studies a lower ratio in postmenopausal women with breast cancer. Research is ongoing inasfar the determination of estradiol metabolites also in blood or directly in the breast tissue by means of sensitive laboratory methods may allow predictive statements. However, it has be to consider that estradiol metabolism can be influenced by external factors such as nutrition, smoking, sports and drugs such as L-thyroxine and H2-antagonists. We were able to demonstrate that estradiol metabolism during estradiol treatment depends on the application mode and might be differently influenced by addition of the various progestins. Whether the investigation of gene polymorphism of enzymes, which are involved in estradiol metabolism, may be helpful for the assessment or treatment of risk patients, to our opinion needs further research.

2-Methoxyestradiol↗
PubMed2004

17beta-estradiol prevents blood-brain barrier disruption induced by VEGF.

We performed this study to determine how pretreatment of the ovariectomized rats with 17beta-estradiol could affect blood-brain barrier disruption caused by the vascular endothelial growth factor (VEGF), an important mediator of vascular permeability. Ovariectomized female rats aged twelve to fourteen weeks were used in the study. A 500 micro g 17beta-estradiol 21-day release pellet was implanted in the 17beta-estradiol group, and a vehicle pellet was implanted in the control group 21 days before the experiments. We performed three craniotomies under isoflurane anesthesia to expose cerebral cortices. Normal saline, 10 (- 10)M and 10 (- 9)M VEGF patches were applied on each hole for 30 min. The transfer coefficient (Ki) of (14)C-alpha-amino isobutyric acid and volume of (3)H-dextran (70,000 dalton) distribution were determined to measure the degree of BBB disruption. Ki was increased by 108 % and 138 % with 10 (- 10)M and 10 (- 9)M VEGF respectively after VEGF application in the control group (p < 0.01). However, there was no significant increase in the Ki with the VEGF application in the 17beta-estradiol group, and their values were significantly lower than the corresponding data of the control group (10 (- 10)M: - 55 %, 10 (- 9)M: - 52 %, p <0.05). The volume of dextran distribution in the control group increased by 47 % with VEGF 10 (- 9)M (p < 0.05), whereas there was no significant change in the volume of dextran distribution with VEGF application in the 17beta-estradiol group and the volume was lower than the corresponding volume of the vehicle-treated control group (10 (- 10)M: - 34 %, 10 (- 9)M: -32 %, p < 0.05). In conclusion, our study demonstrated that chronic 17beta-estradiol treatment prevented BBB disruption induced by the VEGF in the ovariectomized rats.

Animals↗
PubMed2004

Lipid peroxidation at various estradiol concentrations in human circulation during ovarian stimulation with exogenous gonadotropins.

The aim of our study was to investigate the correlation between serum malondialdehyde levels and serum estradiol concentrations in healthy human female subjects. Nine hundred and fifty-five blood samples, from infertile women undergoing controlled ovarian hyperstimulation treatment with recombinant follicle-stimulating hormone, were collected for estradiol and malondialdehyde measurements. Five groups were formed according to serum estradiol levels: Group I (< 50 pg/ml), group II (50 - 299 pg/ml), group III (300-999 pg/ml), group IV (1000-1999 pg/ml) and group V (> or = 2000 pg/ml). One-way analysis of variance was used for comparisons. Mean malondialdehyde concentrations were 1.74 +/- 0.24 mmol/ml (group I), 1.53 +/- 0.20 mmol/ml (group II), 1.69 +/- 0.24 mmol/ml (group III), 1.77 +/- 0.21 mmol/ml (group IV) and 1.86 +/- 0.20 mmol/ml (group V), respectively. Mean serum malondialdehyde level at physiological estradiol concentrations (50-199 pg/ml, group II) was significantly (p < 0.01) lower than the mean malondialdehyde levels in other groups. Mean malondialdehyde concentrations among the remaining groups did not significantly differ. Our findings suggest that in vivo lipid peroxidation might be increased when circulating estradiol concentrations are below (< 50 pg/ml) or above (> 300 pg/ml) the physiological limits. High blood estradiol levels in human female subjects during ovarian stimulation with exogenous gonadotropins could be associated with increased serum malondialdehyde concentrations.

Adult↗
PubMed1994

Triiodothyronine and estradiol increase the serum level of androstanediol glucuronide but do not influence androgen UDP-glucuronyl transferase activity in the female rat.

In this study, adult female rats were treated with either estradiol, testosterone or triiodothyronine (T3). The mean +/- SD for serum levels of androstane-3 alpha,17 beta-diol glucuronide (ADIOL-G) in rats injected with estradiol (31.1 +/- 6.1 nmol/l) and T3 (28.7 +/- 6.1 nmol/l) increased three-fold in comparison to the controls (9.2 +/- 3.6 nmol/l; p < 0.01). There was no significant increase in ADIOL-G levels in rats injected with testosterone (12.0 +/- 3.4 nmol/l) even though serum testosterone levels increased more than 17-fold (1.2 +/- 0.3 nmol/l; p < 0.01). Testosterone levels remained below the detection level of the assay (0.07 nmol/l) in the control and the estradiol and T3 treatment groups. Androgen UDPGT activity in liver microsomes was not altered by treatment with testosterone, estradiol or T3. However, the UDPGT activity for p-nitrophenol increased two-fold in estradiol and T3-treated females (p < 0.01), but was not significantly altered by testosterone treatment. These results suggest that the activity of androgen UDPGT in liver is not the limiting factor in the increased serum levels of ADIOL-G observed on treatment with estradiol and T3.

Androstane-3,17-diol↗
PubMed1984

Enhancement in cholesterol-esterase activity and lipolysis due to 17 beta-estradiol treatment in rat adipose tissue.

The effects of 17 beta-estradiol and testosterone administration on cholesterol esterase, lipoprotein lipase activities and adrenalin-induced lipolysis were examined in rat adipose tissues with the change in serum lipid level. The administration of 17 beta-estradiol (500 micrograms/kg, 2 or 4 weeks) to male rats significantly reduced the body weight, and markedly increased serum cholesterol, triacylglycerols and phospholipids. Cholesterol esterase activity was significantly enhanced in the epididymal adipose tissue from estradiol treated rats and the effect was greater with duration of the treatment. In contrast, lipoprotein lipase activity was markedly reduced. Testosterone reduced cholesterol esterase activity in the parametrial adipose tissue through the treatment with 500 micrograms/kg for 6 weeks, but it did neither influence serum lipids nor lipoprotein lipase activity. Basal lipolysis and adrenalin-induced lipolysis were also significantly enhanced in the epididymal adipose tissue from the male rat treated either with 7 mg/kg estradiol 12 h ahead or with 500 micrograms/kg estradiol for 2 weeks. These results indicate that estradiol exerts strong effects on metabolism of the adipose and these effects seems to be mediated through cyclic-AMP. An alteration of adrenergic functions by gonadal steroids might be intervened.

Adipose Tissue↗
PubMed1999

Upregulation of thrombomodulin antigen levels in U937 cells by combined stimulation with estradiol-17beta and vitamin K2 (menaquinone 4).

The expression of thrombomodulin (TM) and tissue factor (TF) antigens by estradiol and vitamin K2 were studied in human leukemic cell lines including U937 (monoblastic leukemia), NB4 (acute promyelocytic leukemia), and HL60 (acute myeloblastic leukemia). Combined stimulation with estradiol-17beta and menaquinone 4 (MK4), homologue of vitamin K2, showed a remarkable increase of total TM antigen level only in U937 cells among these leukemic cell lines, whereas a single treatment of each agent showed a modest or a moderate increase. A synergistic effect of cotreatment with estradiol-17beta and MK4 was observed in an optimum concentration of 1.0 micromol of estradiol-17beta and 1.0 micromol of MK4. Estrogen receptors were detected only in U937 cells among these cell lines, and the competitive assay with an antiestrogenic agent showed a suppression on TM expression in a dose-dependent manner. In the mean time, concerning expression of TF antigens, if at all, only a very slight decrease was observed by costimulation with estradiol-17beta and MK4 in U937 and NB4 cells, whereas all-trans-retinoic acid (ATRA) showed a remarkable decrease in surface TF antigen levels in NB4 cells and also a modest decrease in U937 cells. These findings suggest that estradiol-17beta would up-regulate TM antigen expression via estrogen receptors and in cooperation with MK4, showing a different mechanism from ATRA.

Antigens↗

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