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PubMed2004

Validation of a gas chromatography-mass spectrometry method for the determination of pg/ml levels of 17beta-estradiol and 17beta-trenbolone in bovine serum.

A method for the quantitation of pg/ml levels of 17beta-estradiol and 17beta-trenbolone in bovine serum by gas chromatography/electron-capture mass spectrometry has been developed and validated. Using the area ratios of the integrated molecular-ion peaks of the analytes to their corresponding deuterated internal standards, [2,4,16,16-2H4] 17beta-estradiol (17beta-estradiol-d(4)) and [16,16-2H2] 17beta-trenbolone (17beta-trenbolone-d(2)), and non-weighted linear regression, two calibration curves per analyte; 5-50 and 50-500 pg/ml for 17beta-estradiol in sera, and 25-250 and 250-2500 pg/ml for 17beta-trenbolone in sera, respectively, were constructed. Splitless injection of 200 fg 17beta-estradiol and 1000 fg 17beta-trenbolone could be detected and quantified. Tested batches of control bovine sera did not exhibit interference for 17beta-trenbolone, and showed expected background presence of endogenous 17beta-estradiol. Intra-day residual errors did not exceed 20%, and regression correlations were greater than 0.99. Intra-day precision data was similar to inter-day precision data. Using this method, 16 samples can be processed within one working day.

Animals↗
PubMed2006

Fluorescence spectroscopy evaluation of fibrinogen-beta-estradiol binding.

Fluorescence spectroscopy experiments were performed in order to study conformational changes induced by the binding of beta-estradiol to fibrinogen at different ligand concentrations. The association constant (Ka) obtained for the fibrinogen-beta-estradiol binding was 6.47x10(6)M(-1), indicating a high affinity interaction. Fluorescence quenching experiments showed that approximately 30% of the tryptophan residues in the protein quaternary structure are accessible to ionic quenchers. The extent of quenching in the absence and presence of beta-estradiol was maximum for cesium ions and minimum for iodide, suggesting the presence of negatively charged residues in the vicinity of the tryptophan residues. The quenching parameters obtained at different beta-estradiol concentrations show alterations that confirm a conformational change, possibly due to a discrete reorganization of tryptophan residues during fibrinogen-beta-estradiol binding. This binding may be responsible for the effects of beta-estradiol on the decrease of erythrocyte aggregation and on cardiovascular risk reduction.

Databases, Protein↗
PubMed2005

Effects of 17beta-estradiol on matrix metalloproteinase-1 synthesis by human dermal fibroblasts.

BACKGROUND: Hormone replacement therapy (HRT) has been used in treatment of various menopausal disorders. It has been well documented that HRT increases the amount of dermal collagen and skin thickness in vivo. However little is known about the effects of female sex hormones on dermal fibroblasts in vitro. OBJECTIVE: The aim of this study is to determine whether or not 17beta-estradiol affects mRNA expression and production of type I collagen, matrix metalloproteinases-1 (MMP-1), tissue inhibitor metalloproteinases-1 (TIMP-1) or transforming growth factor-beta1 (TGF-beta1) by human dermal fibroblasts. METHODS: Fibroblasts were cultured with and without 17beta-estradiol for 6h. We evaluated the changes of mRNA expressions and protein production of type I collagen, MMP-1, TIMP-1 and TGF-beta1. RESULTS: The mRNA expressions of collagen alpha1(I), MMP-1, TIMP-1, TGF-beta1 were not changed by 17beta-estradiol stimulations at a concentration of 10(-12) to 10(-8) M. However, 17beta-estradiol at concentrations of 10(-12) and 10(-10) M exhibited inhibitory effects on proMMP-1, but not type I collagen or TIMP-1 synthesis. The synthesis of TGF-beta1 by fibroblasts stimulated with 10(-8) M of estradiol was significantly increased as compared with the control. However, the level of TGF-beta type II receptor phosphorylation was not elevated under the same conditions. CONCLUSION: Suppressed synthesis of MMP-1 at a low concentration of 17beta-estradiol may be partly involved in the dermal tissue remodeling to inhibit the degradative change.

Adult↗
PubMed2005

Comparison of possible carcinogenic estradiol metabolites: effects on proliferation, apoptosis and metastasis of human breast cancer cells.

OBJECTIVES: Certain estradiol metabolites may play a pivotal role in breast carcinogenesis. Of special interest are the metabolites 2-hydroxyestradiol (2-OHE2), which can react anti-carcinogenically, and 4-hydroxyestradiol (4-OHE1) and 16a-hydroxyestrone (16-OHE1), which may have procarcinogenic potential. In the present study, we have compared for the first time the effect of these metabolites and their parent substance 17beta-estradiol (E2) on proliferation, apoptosis, apoptosis markers and markers of metastatic property of human breast cancer cells. METHODS: MCF-7 cells (human estrogen-receptor positive metastatic breast cancer cell line) were incubated with the estrogens at concentrations of 0.1-100 nM. Cell proliferation rate was measured by the ATP-assay. Apoptosis was measured by cell death assay and the apoptosis markers cytochrome C, Bcl-2, Fasl and p53 were determined in cell lysates by ELISAs. The markers of metastatic property of the cell line, VEGF and MCP-1 were measured in the cell supernatant by ELISAs. RESULTS: The estrogens E2, 4-OHE2 and 16-OHE1 display a proliferative effect on MCF-7 cells which is accompanied by a down-regulation of apoptosis. Various markers of apoptosis such as Bcl-2, cytochrome C and p53 appear to be involved. No significant effect was found for the metabolite 2-OHE2. VEGF and MCP-1 were up-regulated by E2 and 16-OHE1, whereas 2-OHE2 and 4-OHE2 did not show any effect. CONCLUSIONS: The most potent estrogen regarding proliferation, apoptosis and metastasis of breast cancer cells seems to be estradiol. However, the estradiol metabolites 4-OHE2 and 16-OHE1 elicit similar properties on cell proliferation, apoptosis and metastasis as compared to estradiol but only at higher concentrations. In contrast 2-OHE2 did not show any significant effect on these parameters. Thus, intracellular estradiol metabolism may determine an individual's risk for breast carcinogenesis.

Apoptosis↗
PubMed2006

Estradiol affects androgen-binding protein expression and fertilizing ability of spermatozoa in adult male rats.

The estrogenicity of certain environmental pollutants is being increasingly correlated to decline in sperm counts and fertility of the males. Qualitative effects, if any, of estrogen(s) on terminal differentiation of spermatids have been less reported. The present study suggests that exposure to estrogen(s) can also alter the status of condensed chromatin in testicular spermatozoa and reduce their fertilizing potential. A significant reduction was evident in the serum gonadotropins, testosterone, weights of reproductive organs, sperm counts and litters sired by male rats after 10 days of estradiol exposure to a dose of 0.1mg/kg/day. Estradiol treatment led to retardation of in vitro decondensation rates of sperm chromatin, reduction in the uptake of acridine orange dye by chromatin, reduction in susceptibility of chromatin to acid denaturation in vitro, reduced uptake of thiol reactive monobromobimane dye and reduced levels of immunoreactive protamine 1 in caput epididymal sperms. Concomitantly, testicular levels of immunoreactive protamine 1, transition proteins 1/2 and cyclic adenosyl response element modulator-tau (CREMtau) were significantly reduced whilst their mRNA levels were unaffected after estradiol treatment. A significant increase was observed in the testicular mRNA levels of androgen-binding protein (ABP) in estradiol treated sires. An inverse correlation was observed between ABP mRNA levels and uptake of acridine orange by estradiol treated caput sperm chromatin. The results suggest that estradiol-induced increase in ABP mRNA underlies the mechanism(s) involved in the reduction in levels of certain proteins involved in nuclear chromatin condensation during spermiogenesis.

Androgen-Binding Protein↗
PubMed2004

Tissue-specific effect of estradiol on endothelial cell-dependent lymphocyte recruitment.

Estrogen profoundly affects onset and severity of many immune-mediated diseases. In our murine model of drug-induced autoimmunity, female-specific, estrogen-dependent increase in splenic lymphocyte homing was directly implicated in increased disease severity. The present study evaluated the effect of estradiol on microvascular endothelial cells from the spleen compared to endothelial cells from the dermis, which has no disease manifestation in this model. Estradiol increased spleen endothelial cell estrogen receptor (ER) alpha 2.9-fold and decreased estrogen receptor beta 2.1-fold while decreasing both receptors on dermal cells. Estradiol enhanced adhesion of D10 cells to spleen but not dermal endothelial cells 1.53-fold (P < 0.001), an increase that was inhibited by antibodies to VCAM-1 and ICAM-1, and by the estrogen receptor antagonists tamoxifen and ICI 182,780. Estradiol induced greater VCAM-1 expression on spleen than dermal endothelial cells (P < 0.05). Estradiol increased spleen endothelial cell estrogen receptor alpha 2.9-fold and decreased estrogen receptor beta 2.1-fold while decreasing both receptors on the dermal cells. Estrogen specifically and preferentially promoted spleen chemokine protein expression for MCP-1 and MCP-3, while having no effect on dermal protein expression for these chemokines. Estradiol-mediated effects on splenic chemokines were abrogated by tamoxifen and ICI 182,780. The gender-specific increase in lymphocyte homing to spleen may be attributable, at least in part, to tissue-specific estrogen-mediated effects on microvascular endothelial cells.

Animals↗
PubMed2006

Transcription of estrogen receptor alpha and beta in mouse cerebral cortex: effect of age, sex, 17beta-estradiol and testosterone.

Estrogen actions are mainly mediated by estrogen receptor (ER)alpha and ERbeta which in turn are regulated by several factors including age, sex and gonadal steroid hormones 17beta-estradiol and testosterone. In the present study, we have used nuclear run-off assay to examine the effect of these factors on the rate of transcription of ERalpha and ERbeta of mouse cerebral cortex. The run-off assay result was further corroborated with the measurement of steady state level of ERalpha and ERbeta mRNA by semiquantitative RT-PCR method. Our results reveal that ERalpha transcription rate decreases in old mice of both sexes, whereas ERbeta transcription rate decreases only in old females when compared to their adult counterparts. 17beta-Estradiol supplementation reduces the transcription rate of ERalpha and ERbeta in all groups except in adult male while testosterone treatment down regulates the transcription rate of ERalpha and ERbeta in all groups. The semiquantitative RT-PCR analysis reveals that the level of ERalpha mRNA decreases in old male but shows no effect in old female as compared to adult counterpart. In contrast, ERbeta transcript level decreases in old mice of both sexes. Furthermore, ERalpha mRNA level is higher in adult female than in adult male but no sex-dependent difference is seen in ERbeta mRNA level. Supplementation of 17beta-estradiol shows no significant alteration but testosterone reduces the ERalpha level in male mice, while 17beta-estradiol and testosterone down regulate the ERalpha level in female mice of both ages. In case of ERbeta, 17beta-estradiol decreases the transcript level in all groups except adult male while testosterone treatment results in the down regulation of transcript level in all groups. Thus these findings suggest differential effects of age, sex, 17beta-estradiol and testosterone supplementation on the transcription of mouse ER genes which may account for differences in the protein levels of ERalpha and ERbeta and their functions in the brain.

Aging↗
PubMed2006

Protective effect of 17-beta-estradiol in human neurocellular models of lead exposure.

The developing nervous system has long been recognized as a primary target site for lead (Pb)-induced toxicity. Pb-exposure causes cognitive dysfunction, growth retardation, hyperactivity and neurochemical deficits in animals and humans. In the present study the effects of 17-beta-estradiol on human SH-SY5Y neuroblastoma cells in culture exposed to low-levels of Pb were assessed. The cells were exposed to Pb (0.01-10 microM) for 48 h and cell proliferation was determined by the MTT reduction assay. Pb significantly inhibited the proliferation and growth of neuroblastoma cells in a concentration-dependent manner. A 50% inhibition (IC50) in the proliferation of cells was observed with 5 microM Pb. Exposure of cells to Pb (5 microM) for 48 h resulted in a significant increase (+732% of control) in caspase-3 activity, an indicator of apoptosis and total cellular prostaglandin E2 level (+1180% of control), marker of programmed cell death/neuronal cell loss. Pretreatment with 17-beta-estradiol (10 nM) effectively blocked the effects of Pb on caspase-3 activity but not prostaglandin E2 level. Further, Pb but not 17-beta-estradiol in a concentration (0.1-10 microM)-dependent manner effectively decreased (38-84%) the cellular concentration of glutathione (GSH), an important intracellular antioxidant. However, the effect of Pb on GSH level was effectively blocked when pretreated with 17-beta-estradiol. The data indicate that even low concentrations of Pb can be detrimental and potentially toxic to the developing brain. In conclusion, these results suggest that at least some of the neurotoxic effects of Pb may be mediated by apoptosis, which by pretreatment with 17-beta-estradiol can be prevented. This study further confirms previous reports of 17-beta-estradiol acting as a neuroprotective and antiapoptotic agent during induced toxic stress conditions.

Antioxidants↗
PubMed2006

Estradiol increases consumption of a chocolate cake mix in female rats.

Female Sprague-Dawley rats were given an opportunity to eat chocolate cake mix (CCM) using a common brand of cake mix, while standard laboratory food was also available. They took large amounts of the CCM, often taking more than 20 g in 24 h. Some animals were given a single injection of 1 of 6 doses of estradiol valerate (ranging from 0.09 to 10.0 mg/kg) and others were given vehicle. Estradiol valerate provides for sustained release of estradiol. Those receiving estradiol ate more than those receiving vehicle at doses larger than 0.09 mg/kg. Further, with a dose of 10 mg/kg, greater intake among estradiol-treated females was apparent 2 months post-injection. Methodological issues of neophobia and conditioned avoidance were addressed in the study's design and may explain why increased intakes were observed here in contrast to the consensus that estradiol reduces food intake.

Animals↗
PubMed2004

Short-term transdermal estradiol therapy, cognition and depressive symptoms in healthy older women. A randomised placebo controlled pilot cross-over study.

The potential role of estrogen in protecting women from cognitive decline and reducing depressive symptoms is of great therapeutic interest. In a pilot randomised placebo controlled cross-over study, we aimed to determine the short-term effects of transdermal estradiol therapy on cognition and depressive symptoms in healthy cognitively normal post-menopausal women over 60 years of age. Nineteen cognitively normal women, without clinical depression whom had undergone a hysterectomy in the past were recruited. Women were randomised to receive either transdermal estradiol 50 microg/24 h (Femseven) or transdermal placebo for 12 weeks before crossing over to the other medication for a further 12 weeks. Cognition was assessed every 6 weeks by the cognitive drug research (CDR) computerised assessment which recorded both accuracy and speed in the following cognitive tests; simple reaction time, choice reaction time, digit vigilance, visual tracking, spatial working memory, immediate and delayed word recall and delayed face and picture recall. Depressive symptoms were measured using the brief assessment scale depression card (BASDEC) depression rating scale at baseline, 12 and 24 weeks. Participants had a mean age of 71, IQ of 115 and MMSE of 29. Simple reaction time and the BASDEC depression rating scale improved after 12 weeks of estradiol use. All other tests were unaltered by estradiol. Twelve weeks of transdermal estradiol therapy did not consistently improve the speed or accuracy of older women in various cognitive tests. However, the results do support the concept that depressive symptoms may be reduced by estradiol, and not simply due to the relief of climacteric symptoms.

Administration, Cutaneous↗
PubMed2004

Involvement of atrial natriuretic peptide in blood pressure reduction induced by estradiol in spontaneously hypertensive rats.

The aim of the present study was to determine the involvement of atrial natriuretic peptide (ANP) in blood pressure (BP) alterations induced by estradiol treatment. Spontaneously hypertensive rats (SHR) and Wistar rats (WR) were ovariectomized and, after 3 weeks, were injected daily for 4 days with estradiol benzoate (E2; 5 microg/100 g/day) or a vehicle. One day after the last injection, the animals were decapitated, blood was collected, and both right and left atrial appendages were quickly removed for determination of ANP by radioimmunoassay (RIA), or used for ANP mRNA determination. Estradiol treatment induced a significant reduction of blood pressure in SHR, but not in WR. This reduction was correlated with the increase of plasma ANP levels that were significantly increased in E2-treated, compared with vehicle-treated, SHR. E2-treated SHR showed significant increases in ANP concentration in the right and left atria compared to the vehicle-treated animals. These observations were confirmed by ANP mRNA. In summary, the present study shows that short-term estradiol treatment reduces the blood pressure of ovariectomized SHR, but not of WR. This reduction was highly correlated with increased plasma estradiol and ANP levels. These results suggest that ANP is involved in mediating the effect of estradiol on blood pressure reduction.

Animals↗
PubMed2005

Plasma concentrations of estradiol in women suffering from schizophrenia treated with conventional versus atypical antipsychotics.

BACKGROUND: Low estrogen levels leading to an elevated rate of menstrual dysfunctions such as amenorrhea and irregular menstruation have been described in women with schizophrenia and have often been attributed to antipsychotic-induced hyperprolactinemia. However, there is some evidence that "hypoestrogenism" in schizophrenic women does not occur exclusively under medication with hyperprolactinemia-inducing antipsychotics. While the precise mechanism of low estrogen levels in schizophrenic women has not been elucidated yet, "hypoestrogenism" is of clinical relevance because estrogen seems to endow an antipsychotic-like effect in schizophrenia and thus positively affect the course of illness in schizophrenic women. In addition, low levels of estrogen might have a negative effect on bone mineral density and on the cardiovascular system. METHODS: To test the "hypoestrogenism hypothesis", hormone levels in 75 women with schizophrenia diagnosed according to DSM-IV and ICD-10 were determined in the follicular, periovulatory, and luteal phases of the menstrual cycle. Levels of estradiol, prolactin, luteinizing hormone (LH), follicle-stimulating hormone (FSH), progesterone, and testosterone were assessed. RESULTS: The serum levels of estradiol were generally reduced during the entire menstrual cycle compared to normal reference values. With low levels of LH over the entire cycle and of progesterone in the luteal phase, anovulatory cycles were assumed. Hypoestrogenism was found in about 60% of the patients in accordance with a strict definition (estradiol serum level below 30 pg/ml in the follicular phase and below 100 pg/ml in the periovulatory phase). To rule out a possible effect of hyperprolactinemia on the gonadal axis and a subsequent effect on estradiol levels from treatment with conventional ("typical") antipsychotics, serum estradiol levels of patients treated with certain atypical antipsychotics known to induce only a mild increase in prolactin, or no increase at all, were compared with those from patients treated with conventional antipsychotics. The data clearly indicate high prolactin levels in the latter, but low levels in the group treated with atypical antipsychotics. In both groups, however, low levels of estradiol compared to normal reference values were measured. CONCLUSIONS: The present findings provide evidence that hypoestrogenism in schizophrenia occurs in women with and without antipsychotic-induced hyperprolactinemia. Further research should be conducted to clarify the cause of hypoestrogenism in schizophrenic women and focus on possible clinical implications.

Adolescent↗
PubMed2005

Modulation of vitellogenin synthesis through estrogen receptor beta-1 in goldfish (Carassius auratus) juveniles exposed to 17-beta estradiol and nonylphenol.

Many synthetic chemicals, termed xenoestrogens, have been shown to interact as agonists with the estrogen receptor (ER) to elicit biological responses similar to those of natural hormones. To date, the regulation of vitellogenesis in oviparous vertebrates has been widely used for evaluation of estrogenic effects. Therefore, Carassius auratus juveniles were chosen as a fish model for studying the effects of estradiol-17beta and different concentrations (10(-6) and 10(-7) M) of 4-nonylphenol (4-NP) on the expression of liver ERbeta-1 subtype; plasma vitellogenin and sex steroids (androgens and estradiol-17beta) were also evaluated together with the bioaccumulation process, through mass-spectrometry. C. auratus is a species widespread in the aquatic environment and, on the toxicological point of view, can be considered a good "sentinel" species. Juveniles of goldfish were maintained in tanks with only tap water or water with different concentrations (10(-6) and 10(-7) M) of 4-nonylphenol (4-NP), or 10(-7) M of estradiol-17beta. After 3 weeks of treatment, animals were anesthetized within 5 min after capture, and blood was immediately collected into heparinized syringes by cardiac puncture and stored at -70 degrees C; the gonads were fixed, then frozen and stored at -70 degrees C; the whole fish, liver, and muscle tissues were harvested and immediately stored at -70 degrees C for molecular biology experiments and bioaccumulation measurements. The estrogenic effects of 4-NP were evidenced by the presence of plasma vitellogenin in juveniles exposed both to estradiol-17beta and the two doses of 4-NP; moreover, exposure to 4-NP also increased aromatization of androgens, as suggested by decreasing androgens and increasing estradiol-17beta plasma levels. The changes of these parameters were in agreement with the increasing transcriptional rate of ERbeta-1 mRNA in the liver, demonstrating that both estradiol-17beta and 4-NP modulate the vitellogenin rate through interaction with the ERbeta-1 subtype. The present study also suggests that 4-NP at the concentration of 10(-6) M bioaccumulates in the liver.

Androgens↗
PubMed2004

Interrelationships of estradiol, inhibin, and gonadotropins during follicle deviation in pony mares.

The changes in circulating concentrations of FSH, LH, estradiol, and total inhibin associated with the beginning of follicle diameter deviation were compared among the last anovulatory follicular wave of the year and the first and second ovulatory waves in pony mares ( n=7 ). Follicle diameters and circulating hormone concentrations for each wave were normalized to the observed beginning of deviation (Day 0). Follicle deviation was demonstrated during the anovulatory wave as well as during the ovulatory waves, and the diameter of the future dominant follicle at the beginning of deviation was similar for the three waves (overall mean: 23.7+/-0.6 mm). Circulating estradiol concentrations did not increase during the last anovulatory wave but increased similarly for the two ovulatory waves, beginning near the onset of deviation. There were no differences among waves in concentrations of inhibin encompassing deviation. The FSH concentrations for the wave-stimulating FSH surge did not differ significantly among the three waves; combined for the three waves, concentrations decreased between Days -3 and 7. Circulating LH did not increase during the last anovulatory wave but increased during the first and second ovulatory waves beginning on Days 6 and -2, respectively. Results indicated that the increase in circulating estradiol at the beginning of deviation was not required for suppression of the wave-stimulating FSH surge and the initiation of deviation, based on an estradiol increase in association with deviation during the ovulatory waves but not during the anovulatory wave. Concentrations of inhibin were similar among waves and, therefore on a temporal basis, the similar suppression of FSH was attributable to inhibin. The later increase in LH before the first ovulation was not attributable to estradiol, based on the similarity between the two ovulatory waves in the increasing estradiol concentrations.

Animals↗
PubMed2004

Different effects of subchronic doses of 17-beta estradiol in two ethologically based models of anxiety utilizing female rats.

Estrogen may have differing effects on 'anxiety' responses under different conditions. The current study tested the effects of estrogen on anxiety-like behavior when administered for 6-7 days in ovariectomized (OVX) female rats. Two animal paradigms were utilized; the elevated plus maze (EPM), measuring changes in innate fear of exploration of open spaces; and the social interaction test (SIT), measuring the exploration of a novel, same gender partner. In the EPM, estradiol-treated OVX females both entered and spent more time in the open arms than control OVX females, indicating an anxiolytic-like action of estradiol. In contrast, estradiol treated OVX females interacted less with the partner animal in the SIT compared with controls suggesting anxiogenic-like effects. The possible anxiogenic effect of estradiol in the SIT is supported by two findings: (1) the effect is reversed by the anxiolytic drug alprazolam and (2) estrogen did not affect locomotion and therefore, the reduced social interaction is not due to reduced activity. Acute administration of progesterone (5 mg/kg), which has anxiolytic properties, did not reverse estradiol-induced social interaction deficits, suggesting that lack of progesterone did not account for estradiol's anxiogenic effects. These results, while seemingly contradictory when interpreted within a unified concept of anxiety, may well reflect the ethological roles of reproductive hormones and their effects on different types of exploratory anxiety.

Alprazolam↗
PubMed2005

Castration reduces male testosterone, estradiol, and territorial aggression, but not paternal behavior in biparental dwarf hamsters (Phodopus campbelli).

Biparental male hamsters, Phodopus campbelli, act as midwives during the birth of their litter and are highly responsive to an experimentally displaced pup. They also have high peripheral concentrations of estradiol, a hormone with known roles in maternal behavior. Surgical castration during the gestation of their first litter was used to investigate the source of that estradiol and the functional role of testicular sex steroids in paternal responsiveness. In Experiment I, castration reduced both testosterone and estradiol concentrations, confirming that the testes were the primary source of estradiol. However, neither paternal responsiveness nor multiple measures of reproductive success were altered by the castration. Aggression directed towards an intruder, however, was reduced by castration. In Experiment II, removal of prior experience with birth or pups also failed to alter paternal responsiveness in castrated males. Although the present results do not preclude a role for local estradiol synthesis in the brain, results do not support an association between high circulating estradiol in males and their paternal behavior.

Aggression↗
PubMed2006

Social regulation of plasma estradiol concentration in a female anuran.

The behavior of an individual within a social aggregation profoundly influences behavior and physiology of other animals within the aggregation in such a way that these social interactions can enhance reproductive success, survival and fitness. This phenomenon is particularly important during the breeding season when males and female must synchronize their reproductive efforts. We examined whether exposure to conspecific social cues can elevate sex steroid levels, specifically estradiol and androgens, in female túngara frogs (Physalaemus pustulosus). We compared plasma estradiol and androgen concentrations in wild-caught females before and after exposure to either natural mate choruses or random tones. After exposure to mate choruses for 10 consecutive nights, estradiol concentrations were significantly elevated whereas there was no significant elevation in estradiol concentrations in the group of females exposed to random tones for 10 nights. Plasma androgen concentrations were not significantly changed after exposure to either natural mate choruses or random tones for 10 consecutive nights. Social modulation of estradiol concentrations may be important in maintaining a female's reproductive state while males are chorusing. To our knowledge, this is the first study to demonstrate social regulation of estradiol concentration in female anurans.

Acoustic Stimulation↗
PubMed2000

The effects of transdermal estradiol on the response to mental stress in postmenopausal women: a randomized trial.

PURPOSE: Estrogens inhibit adrenomedullary catecholamine release and catecholamine-mediated responses to stress. We examined whether estrogen supplementation reduces the sympathoadrenal response to mental stress in postmenopausal women. MATERIALS AND METHODS: We compared the effects of 3-week treatment with transdermal 17-beta-estradiol and placebo in 10 postmenopausal women using a randomized, blinded, crossover design. We measured plasma catecholamine levels and the cardiovascular and metabolic responses to a 15-minute stress with mental arithmetic. Treatments were compared using repeated measures analysis of variance. RESULTS: During placebo treatment, mean (+/- SD) epinephrine levels reached a peak of 431 +/- 135 pmol/liter after 15 minutes of stress; the epinephrine response was blunted during estradiol treatment, with a peak of 357 +/- 77 pmol/liter (P <0.05). Estradiol also blunted the diastolic blood pressure response to stress (baseline levels of 78 +/- 15 mm Hg vs peak of 90 +/- 6 mm Hg during placebo; baseline of 80 +/- 8 mm Hg vs peak of 84 +/- 6 mm Hg during estradiol; P <0.05). Estradiol treatment also blunted the decrease in the standard deviation of the mean of the electrocardiographic RR intervals and the increase in the ratio between the low-frequency and high-frequency bandwidths. CONCLUSION: We observed a moderate, although significant, reduction in markers of the stress response to mental arithmetic in postmenopausal women treated with transdermal 17-beta-estradiol.

Administration, Cutaneous↗