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At least 19 recordsLinked to original sources

PubMed1989

2- and 4-iodinated estriol as indicator ligands for estriol radioimmunoassays with anti-estriol-C6 conjugate antiserum.

The suitability of 2- and 4-125I-estriol as indicator ligands for estriol determination in radioimmunoassays with anti-estriol-C6 conjugate antiserum was tested and compared to the one of 3H-estriol, estriol-6-(O-carboxymethyl)oxime-125I-histamine and a commercially available 125I-estriol derivative of unknown structure. An ideal radioiodinated tracer would react identically with the analyte and its tritiated analogue and the 4-monoiodo-estriol was found to fulfil these requirements as shown by the pattern of dilution and standard curves obtained with the various labeled ligands. This observation was corroborated by a comparison of the apparent estriol concentrations in human pregnancy sera determined with the different indicator ligands. The experimentally proven advantage of 4-monoiodo-estriol over other iodinated estriol derivatives verifies a hypothesis deduced previously from binding constants obtained with analogous estriol derivatives and the same antiserum.

Animals↗

PubMed1986

Effect of estriol, estriol-3-sulfate and estriol-17-sulfate on progesterone and estrogen receptors of MCF-7 human breast cancer cells.

The levels of progesterone receptors (PR [cytosol (Cy) and nuclear (N)] and estrogen receptors (ER) [cytosol and nuclear; occupied and unoccupied specific binding sites] were evaluated in the MCF-7 cancer cell line incubated with estriol (E3), estriol-3-sulfate (E3-3-S) or estriol-17-sulfate (E3-17-S) for 7 days in culture. Cells were grown in MEM medium containing 2 mM glutamine, 10% v/v dialysed calf serum and penicillin-streptomycin (100 U/ml) in the absence (control) or in the presence of 5 X 10(-8) M E3, E3-3-S or E3-17-S. The total PR (Cy + N) concentration which was 0.47 +/- 0.10 (SE) pmol/mg DNA in the non-treated cells, increased to 1.95 +/- 0.48 in the E3 and to 1.55 +/- 0.26 in the E3-3-S treated cells. No effect (PR: 0.47 +/- 0.15 pmol/mg DNA) was observed with the E3-17-S treatment. Total ER (Cy + N, occupied + unoccupied binding sites) in pmol/mg DNA +/- SE, were as follows: control 0.79 +/- 0.17; + E3: 0.33 +/- 0.09; +E3-3-S: 0.90 +/- 0.18 and +E3-17-S: 1.82 +/- 0.58. The measurement by radioimmunoassay of unconjugated estriol in the culture medium indicated that after incubation with E3-3-S, a fraction (0.5-1%) of the sulfate was hydrolyzed but no hydrolysis was observed in the incubations with E3-17-S. It is concluded that in the MCF-7 human mammary cancer cell line E3 and E3-3-S stimulate PR very significantly, but it is suggested that E3-3-S acts through the hydrolyzed E3. On the other hand, E3-17-S is inactive because it is not hydrolyzed. Consequently, E3-3-S can play an important role in the biological responses of this mammary cancer cell line.

Breast Neoplasms↗

PubMed1986

Biological effects and morphological responses to estriol, estriol-3-sulfate, estriol-17-sulfate and tamoxifen in a tamoxifen-resistant cell line (R-27) derived from MCF-7 human breast cancer cells.

The R-27 cell line is a variant clone derived from the MCF-7 human breast cancer cell line which has lost its inhibitory response to anti-estrogens. In the present study, we have compared the biological responses to estriol (E3), estriol-3-sulfate (E3-3-S), and estriol-17-sulfate (E3-17-S) in these cells and in the parent MCF-7 cells. In the R-27 cell line after 7 days of culture, the progesterone receptor (PR) concentrations were greatly increased by E3 and E3-3-sulfate; however, tamoxifen did not block this effect. The effect in PR provoked by E3-17-S was significantly less intense. The concentrations of PR (pmol/mg DNA +/- S.D.) in the R-27 cells were as follows: control: 1.1 +/- 0.8; +E3: 10.5 +/- 2.4; +E3-3-S: 5.4 +/- 2.3; +E3-17-S: 2.6 +/- 0.8. E3 and E3-3-S also stimulated PR in the MCF-7 cells but to a lesser extent. No stimulation was observed in the E3-17-S treatment. A fraction (0.5-1%) of the E3-3-S was found to be hydrolysed in the medium during the incubation in both cell lines, but no hydrolysis occurred after incubation with E3-17-S. Ultrastructural observations showed that in the E3 and E3-3-S treated cells, there was an important development of the ergastoplasm, bundles of filaments and an accumulation of ribosomes. No significant morphological alteration was observed in cells exposed to E3-17-S. In conclusion, E3 is biologically very active in both the R-27 and the MCF-7 cell lines and E3-3-S could play a role in the control of the estrogenic activity of E3.

Breast Neoplasms↗

PubMed1976

Splanchnic and intestinal uptake and formation of estriol and estriol conjugates in the dog in vivo.

A loading dose of 3H-estriol was given to male dogs followed by a constant infusion. The concentrations of total radioactivity, conjugated estriol metabolites, estriol, estriol-o-glucosiduronate, estriol-16alpha-glucosiduronate, estriol-3-sulfate and estriol-3-sulfate, 16alpha-glucosiduronate were determined in plasma from the femoral artery(A), hepatic vein(HV) and superior mesenteric vein (SMV). From these values the splanchnic (100[1-HV/A]) and intestinal (100[1-SMV/A]) extractions were calculated. The mean splanchnic extraction of total radioactivity was positive (23, SE 3, P less than .01), indicating net uptake by the splanchnic area, possibly due to biliary excretion. The mean splanchnic extraction of estriol was 77, SE 1, P less than .01, also indicating net uptake. The splachnic extractions of estriol-3-glucosiduronate, estriol-16alpha-glucosiduronate and estriol-3-sulfate were negative (-15, SE 3, P less than .01; -23, SE 6, P less than .01; -31, SE 8, P less than .01 respectively) indicating net formation of these conjugates for release into the systemic circulation. The mean intestinal extraction of estriol was 12, SE 4, P less than .01, indicating net uptake by the intestine. This net uptake was associated with mean negative intestinal extractions of estriol-3-glucosiduronate (-15, SE 7, P approximately .05), estriol-3-sulfate (-33, SE 10, P less than .01) and estriol-3-sulfate, 16alpha-glucosiduronate (-53, SE 13, P less than .01), indicating net formation of these conjugates by the intestine.

Animals↗

PubMed1977

Serum free estriol and estriol glucuronide fractions in hydatidiform mole measured by radioimmunoassay.

Serum or plasma total unconjugated estriol and total estriol glucuronide fractions were measured in 14 patients with unaborted hydatidiform mole between 11 and 25 weeks of gestation and in 20 normal pregnant patients between 8 and 17 weeks of gestation. The estriol fractions were separated by solvent partition, and the estriol was measured by radioimmunoassay using antiserum against estriol-16-17-dihemisuccinate conjugated to bovine serum albumin. The values (means and ranges) found in normal pregnant patients were as follows: estriol 1.3 ng/ml (0.3-2.9); estriol glucuronide, 11.1 ng/ml (4.7-24.8). Wide ranges of values were found in patients with molar pregnancies compared to those with normal pregnancies of equivalent gestation, some values being within the upper range of normal and others being well below the normal range. Of the 14 molar pregnancies studied, 9 (64%) were associated with serum estriol values which were below the ranges for normal pregnancy, and 8 (57%) were associated with similarly low estriol glucuronide values. The incidences of low estriol and estriol glucuronide values were less than those reported for low urinary estriol excretion in hydatidiform moles. No correlation was found between any of the serum estriol fractions and the serum hCG values or with the presence of theca lutein cysts in the ovaries. It was suggested that the trophoblast was the principal source of estriol in these molar pregnancies.

Chorionic Gonadotropin↗

PubMed1984

Biology and receptor interactions of estriol and estriol derivatives in vitro and in vivo.

The biological effects of estriol (E3) have been studied in three estrogen targets, namely, the rat uterus in vivo and in vitro, in primary human endometrial cell cultures and in MCF-7 human breast cancer cells in culture. Studies on the temporal relationships between estrogen receptor binding and biological responses in the uterus using estriol and several more long-acting estriol derivatives, namely, 17 alpha-ethynyl estriol, estriol-3-cyclopentyl ether, and 17 alpha-ethynyl estriol-3-cyclopentyl ether, indicate that estriol is a short-acting compound with a brief duration of action. Estriol is a poor stimulator of uterine growth and plasminogen activator activity in vivo. Chemical modifications of the estriol molecule produce long-acting derivatives that result in a prolonged input of hormone receptor complexes into the nucleus and a prolonged and marked stimulation of uterine growth. In human endometrial cells in primary tissue culture, E3 has 12% the affinity of estradiol (E2) for cytosol estrogen receptor and it is quite effective yet slightly less potent than estradiol in stimulation of progesterone receptor synthesis. Low concentrations of E3 (10(-10) M) stimulate growth of MCF-7 cells in vitro and dose-response curves show E3 to be only slightly less effective than E2. In these endometrial and breast cancer cell systems in vitro, there is no metabolism of E3 while E2 is metabolized to estrone. Hence, estriol is an effective estrogen in vitro. In vivo, it is short-acting, but it can be made a full estrogen agonist when given at a sufficiently high concentration or in a chemically modified form which prolongs its activity by enabling effective concentrations of the compound to be maintained in the blood and in target tissues.

Animals↗

PubMed1983

Estriol and estrone interaction with the estrogen receptor. II. Estriol and estrone-induced inhibition of the cooperative binding of [3H]estradiol to the estrogen receptor.

Kinetic analysis of the estrogen receptor's cooperative equilibrium [3H]estradiol binding (Sasson, S., and Notides, A. C., (1982) J. Biol. Chem. 257, 11540-11545) provides a sensitive method for probing the binding of partial agonists to the estrogen receptor. We studied the effects of estriol and estrone on the positive cooperativity of [3H]estradiol binding to the partially purified, calf uterine estrogen receptor. The receptor was titrated with variable concentrations of [3H]estradiol in combination with estriol or estrone, while maintaining a constant molar ratio of the estriol or estrone to the [3H]estradiol. With either a 4-fold molar excess of estriol or a 25-fold molar excess of estrone above the [3H]estradiol concentrations, the receptor's positive cooperative [3H]estradiol binding was inhibited. The Scatchard plot showed a transition from a convex to a linear curve and a decrease in the Hill coefficient value from 1.61 +/- 0.02 (n = 7) in the absence of estriol or estrone to 1.04 +/- 0.04 (n = 4) in the presence of estriol and 0.99 +/- 0.03 (n = 4) in the presence of estrone. The inhibition of the positive cooperativity of [3H]estradiol binding by estriol or estrone was shown not to be due to isotope dilution of the specifically bound [3H]estradiol by the unlabeled estriol or estrone. These kinetic analyses demonstrate that the positively cooperative equilibrium binding of [3H]estradiol by the receptor, which is characteristic of the receptor's activation process, is eliminated by estriol and estrone and consistent with their partial agonist-antagonist activities observed in vivo.

Animals↗

PubMed1990

Effect of combined treatment with phenylpropanolamine and estriol, compared with estriol treatment alone, in postmenopausal women with stress urinary incontinence.

Twenty-nine postmenopausal women with slight to severe stress urinary incontinence and estrogen deficiency symptoms in the urogenital tract were treated with estriol, p.o. 4 mg once daily, and either phenylpropanolamine (PPA), p.o. 50 mg twice daily, or placebo for periods of 6 weeks according to a randomized double-blind crossover schedule. At urodynamic recordings the maximum urethral closure pressure increased by 22% with combined treatment (p less than 0.001) and an additional effect of PPA to estriol was shown (p = 0.022). The pressure transmission ratio increased, by about 15%, with both treatments (p less than 0.07). The number of leakage episodes was reduced by 28% with combined treatment (p = 0.007), but not with estriol alone (p = 0.08). Both combined treatment and estriol alone reduced significantly (p less than 0.01) the urinary incontinence complaints. Twelve women (43%) preferred combined treatment, while 7 (25%) preferred estriol alone. In women with initially slight to very severe urine loss, combined treatment reduced also (p = 0.02) the amount of urine loss, measured at a standardized physical stress test. Signs of estrogen deficiency in vulva, vagina and urethra were reduced, 75% (p less than 0.001) or 65% (p = 0.001) with estriol given in combination with PPA or alone. Maturation index of both urethral and vaginal epithelium displayed significant changes. It is concluded that the combined treatment, PPA + estriol, by affecting both the muscular and mucosal factor of the urethra, is more effective than estriol alone for treatment of female stress urinary incontinence in the postmenopausal ages.

Double-Blind Method↗

PubMed1980

The metabolism of estriol-3-glucosiduronate and estriol in the rabbit.

Urinary metabolites of [6,7-3H]-estriol-3-glucosiduronate and of [6, 7-3H]-estriol in intact female rabbits were analyzed. The separation of urinary metabolites was performed by countercurrent distribution followed by DEAE-Sephadex A-25 column chromatography. Each conjugate was then hydrolyzed with the enzymes and the aglycone thus liberated was identified. In either case, major urinary metabolites were found to be diconjugates, a considerable part of which was glucosiduronate-N-acetylglucosaminide of 17-epiestriol. In addition, estriol-16-glucosiduronate or monoglucosiduronate of 17-epiestriol was identified as a minor urinary metabolite of [6,7-3H]-estriol. From these results, it was concluded that the greater part of the estriol-3-glucosiduronate was converted to diconjugates and that estriol-3-glucosiduronate was probably an intermediate metabolite in the conversion pathway from estriol to diconjugates in this species.

Animals↗

PubMed1979

Unconjugated and total estriol in human amniotic fluid--changes in the ratios between the two estriol levels with advancing gestational age.

In 172 amniotic fluid samples of the early second and the third trimester from 115 normal pregnancies the concentrations of unconjugated and total estriol were measured by means of radioimmunoassay. The mean concentrations of unconjugated estriol in amniotic fluid rose from 1.22 ng./ml. in the gestational weeks 15-18 to 7.82 ng./ml. in the gestational weeks 37-40, that is 6.4 times the former value. In contrast, the mean concentrations of total estriol in amniotic fluid increased more strongly, namely from 27.51 ng./ml. in the gestational weeks 15-18 to 777.15 ng./ml. in the gestational weeks 37-40, that is 28.3 times the former value. With advancing pregnancy the proportion of unconjugated estriol to total estriol in amniotic fluid fell, obeying a significant correlation, from 4.43% in the gestational weeks 15-18 to 1.01% in the gestational weeks 37-40. The presumable reasons for this are the rising conjugation rate of estriol excreted with fetal urine, concomitant to fetal maturation, and the relative transfer diminution of unconjugated estriol from maternal plasma into amniotic fluid with the advance of gestation.

Amniotic Fluid↗

PubMed1983

Estriol and estrone interaction with the estrogen receptor. I. Temperature-induced modulation of the cooperative binding of [3H]estriol and [3H]estrone to the estrogen receptor.

We investigated the calf uterine estrogen receptor's interaction with [3H]estriol and [3H]estrone and found that the receptor's cooperative binding is markedly dependent upon temperature and receptor concentration. With increasing temperature, the intensity of the estrogen receptor's cooperativity decreases: at 0 degrees C the Scatchard plot was convex and the Hill coefficient was 1.58 +/- 0.04 (n = 5), while at 30 degrees C the Scatchard plot approached linearity and the Hill coefficient was 1.03 +/- 0.02 (n = 3) for the binding of [3H]estriol with a receptor concentration of 10 to 12 nM. With increasing receptor concentration, the receptor's cooperativity gradually increased. At a receptor concentration of 1 nM, at 25 degrees C, with [3H]estriol the Hill coefficient was low, 1.03 +/- 0.02 (n = 3), while at approximately intracellular receptor concentration (20 nM) the Hill coefficient increased to 1.20 +/- 0.04 (n = 4). Similar results were observed with [3H]estrone. The cooperative interaction of the estrogen receptor with [3H]estriol or [3H]estrone is reversible and dependent upon temperature. The van't Hoff analysis of the apparent dissociation constant of the [3H]estrone- and [3H]estriol-receptor complexes indicates that a transition in the receptor's binding mechanism occurs at 15 degrees C. Therefore, measurements of ligand interactions with the estrogen receptor at 0 to 15 degrees C, may not reflect the binding mechanism of the receptor at more biologically relevant temperatures. The reduced, positively cooperative interactions of [3H]estriol and [3H]estrone with the estrogen receptor at 30 degrees C, in comparison with estradiol, decrease the presence of the activated receptor, which correlates with the partial agonist-antagonist activities of estriol and estrone observed in vivo.

Animals↗

PubMed1980

Plasma estriol and its conjugates following oral and vaginal administration of estriol to postmenopausal women: correlations with gonadotropin levels.

A study was designed to compared the metabolic fate and the biologic effects of 4 mg of estriol (E3) administered either orally or vaginally to six postmenopausal women. Blood samples were collected every hour for 6 hours and five different estriol fractions as well as gonadotropins were measured. Vaginal E3 administration resulted in a decline of 45% in luteinizing hormone (LH) levels and 17% in follicle-stimulating hormone (FSH) levels at 6 hours after treatment (p < 0.05). In contrast, the administration of 4 mg of E3 orally did not produce a decline of LH and FSH, despite the fact that the serum levels of E3-3-sulfate, E3-3-sulfate-16-glucosiduronate, estriol-3-glucosiduronate, and estriol-16-glucosiduronate were all fourfold to 24-fold higher after oral administration than after vaginal estriol administration. However, since the levels of unconjugated E3 were higher after the vaginal than after the oral administration of estriol, we conclude that only unconjugated E3 suppresses gonadotropins.

Administration, Oral↗

PubMed1977

Maternal serum unconjugated estriol and urine estriol concentrations in normal and high-risk pregnancy.

Serum unconjugated estriol levels and urinary estriol levels of concurrent specimens were compared for 6 normal and 6 high-risk subjects throughout the last trimester of pregnancy. Free estriol values in serum exhibited a close correlation with urinary estriol values for both the normal (r = 0.91) and high-risk (r = 0.92) groups. The results of this study indicate that the assessment of high-risk pregnancies now accomplished principally by urinary estriol assays may be performed by more convenient and rapid radioimmunoassays developed for quantification of free estriol in serum.

Estriol↗

PubMed1977

A rapid radioimmunoassay for serum unconjugated estriol with a directly iodinated estriol radioligand.

Radioiodinated estriol not previously derivatized was found to be immunoreractive and is shown to possess Sephadex-adsorptive characteristics similar to those of tritium-labeled estriol and nonlabeled estriol. Because of these characteristics, radioiodinated estriol is shown to be an acceptable radioligand for use in a rapid and reliable column radioimmunoassay for determination of unconjugated estriol in serum. An evaluation of the estriol column RIA assay with this radioligand is presented.

Chromatography, Gel↗

PubMed1991

Plasma estriol levels after intramuscular injection of estriol and two of its esters.

Twelve female volunteers from Berlin and 9 from Stockholm, all using a contraceptive pill (30 micrograms ethinyl estradiol and 150 micrograms levonorgestrel), received an intramuscular injection of estriol (E3; 1 mg in oil) on day 5 of withdrawal bleeding. Blood samples were collected at increasing time intervals during 4 weeks. Three months later, on day 5 of their withdrawal bleeding, 6 women were given intramuscularly (in oil) estriol 3,17-dipropionate (E3-prop) and 15 women estriol 3,17-dihexanoate (E3-hex). The doses were equivalent to 5 mg of estriol, i.e. 6.94 and 8.90 mg, respectively. Blood samples were collected during a period of 9 weeks. Estriol was analyzed by radioimmunoassay in all plasma samples. The average half-life of E3 ranged from 1.5 to 5.3 h after the administration of E3. It was 12.7 h and between 187 and 221 h after the administration of E3-prop and E3-hex, respectively. The average areas under the curve (in nmol.l-1.h) of E3 were between 82.5 and 161 after the administration of E3-prop or E3-hex, and between 27.1 and 37.9 when E3 had been given. As E3 was administered in a 5-fold lower dose than the esters, the areas under curve appeared to be comparable. Thus, the total exposure to E3 seemed to be almost independent of the type of E3 derivatization, while the time and intensity of exposure were very different.

Adult↗

PubMed1988

Screening in pregnancy with unconjugated serum estriol compared with urinary estriol.

The diagnostic value of estriol determinations in high-risk pregnancies is frequently discussed in the literature. Estriol levels of urine and serum samples of 48 asymptomatic pregnant women were analyzed using direct radioimmunoassay. A correlation was found (r = 0.5997) between urine and serum samples, nevertheless the correlation was stronger (r = 0.8278) if 4 cases with extreme deviation were omitted. In these cases the serum estriol levels were high and the urine estriol levels were low. The outcome of the pregnancies was without any complication. Our observations suggest that determination of unconjugated serum estriol levels is more reliable in the monitoring of high-risk pregnancies, since they do not depend on renal and hepatic functions.

Adult↗

PubMed1981

Relation of estriol in saliva to serum estriol during normal pregnancy.

As saliva is an easily accessible biological material, compared with 24-hour urine and blood, the salivary concentration of estriol was studied from the 30th to the 41st week of gestation in 268 samples from 124 normal pregnancies. At the same time, venous blood samples were drawn and analyzed for total and unconjugated estriol. The mean values for the concentration of total estriol in saliva in the 30th and 41st weeks were 2.8 and 7.2 nmol/l respectively. The salivary estriol concentration appears to increase in perfect conformity with its serum concentration in the course of gestation. If estriol in saliva also reflects low serum values and an impaired function of the feto-placental unit, analyses of the saliva may be applicable as a screening procedure in high-risk pregnancies.

Adolescent↗

PubMed1976

Correlation between morning urine estriol concentration and 24-hour estriol excretion.

In an attempt to circumvent the need for 24-hour urine collections for estriol analyses in assessment of fetal status, the possibility of using morning urine samples was investigated. Results indicate 1) good correlation between 24-hour estriol excretion and morning estriol concentration, and between corresponding E/C ratios, 2) similar morning and 24-hour estriol concentrations, 3) high dependence of estriol and creatinine excretion on 24-hour urine volume but not on morning volume, 4) larger variations in 24-hour than in morning urine volume, and 5) better consistency of values in morning than in 24-hour samples in pathologic pregnancy. The use of serial morning urine concentrations at least as an outpatient monitoring procedure is suggested.

Creatinine↗