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At least 19 recordsLinked to original sources
PubMed1990

Protein binding of active ingredients and comparison of serum ethinyl estradiol, sex hormone-binding globulin, corticosteroid-binding globulin, and cortisol levels in women using a combination of gestodene/ethinyl estradiol (Femovan) or a combination of desogestrel/ethinyl estradiol (Marvelon) and single-dose ethinyl estradiol bioequivalence from both oral contraceptives.

Results from two clinical pharmacokinetic studies are given. The first study was an observational study in oral contraceptive users who took either a combination of gestodene and ethinyl estradiol (pill A, Femovan) or desogestrel and ethinyl estradiol (pill B, Marvelon). A total of 69 women (39 receiving pill A and 30 receiving pill B) were evaluated to determine serum ethinyl estradiol, sex hormone-binding globulin, corticosteroid-binding globulin, and cortisol levels. Samples were obtained on 1 day during the tenth to twenty-first days of pill intake. All women received the respective oral contraceptive for at least 3 months. The test power was such that an 80% difference of 1 standard deviation of each target variable would have been detected (alpha = 0.05; beta = 0.1). No statistically significant differences were found in sex hormone-binding globulin, corticosteroid-binding globulin, or cortisol serum levels between both groups. Time and height of maximum ethinyl estradiol levels were identical as was the area under the curves. Ex vivo protein-binding analysis of the progestins revealed a free portion of 0.6% for gestodene and 2.5% for 3-ketodesogestrel as the active metabolite of desogestrel. Sex hormone-binding globulin-bound portions were much higher for gestodene (75.3% +/- 9.1%) than for 3-ketodesogestrel (31.6% +/- 12%). The remaining fractions were bound to albumin. In a second study, ethinyl estradiol-bioequivalence from pills A and B was investigated in 18 women in a controlled, single-dose, randomized, crossover design. The area under the ethinyl estradiol serum levels were identical up to 4 hours after pill intake between both treatments. According to the relatively low variation in data in this group of women, a 10% difference in ethinyl estradiol-availability could have been detected. Both studies indicate that the pharmacokinetics of ethinyl estradiol were independent of the concomitantly administered progestin, that is, desogestel and gestodene.

Adult↗
PubMed1975

[Estradiol-17beta, estrone, LH and FSH in serum after administration of estradiol-17beta, estradiolbenzoate, estradiol-valeriate and estradiol-undecylate in the female (author's transl)].

Estradiol-17beta, estradiol-benzoate, estradiol-valerianate, and estradiol-undecylate were injected intravenously and intramuscularly to postmenopausal woman and to female castrates. Equal doses were used corresponding to 20 mg of free estradiol-17beta. Estradiol-17beta, estrone, FSH and LH were measured in serum by radioimmunoassay before and after application of the hormone and the estradiol esters. Thus the depot effect of the different esters could be compared.

Adult↗
PubMed2001

Elevation of serum 17-beta-estradiol in channel catfish following injection of 17-beta-estradiol, ethynyl estradiol, estrone, estriol and estradiol-17-beta-glucuronide.

17-beta-Estradiol is naturally converted in numerous organisms to various derivatives/metabolites, which may be excreted from the organism into its immediate external environment. There is a paucity of data regarding the biological effects of these derivatives/metabolites on aquatic organisms. Male channel catfish (200-500 g, N=5, 12-18 months) were injected with 1 mg/kg 17-beta-estradiol (E2), ethynyl estradiol (EE2), estrone, estriol or E2-17-beta-glucuronide with subsequent measurements of vitellogenin (Vtg) and serum E2 concentrations 7 days post injection. EE2 and E2 gave the largest magnitude of Vtg response followed by estrone and estriol. Exposure to EE2, estrone, and E2-17-beta-glucuronide all induced significant increases in serum E2 concentrations. This study indicates that metabolites of E2 are also estrogenic and may potentially disrupt estrogen feedback loops within aquatic organisms.

Journal Article↗
PubMed1990

Plasma estradiol-17 beta concentrations in the cow during induced estrus and after injection of estradiol-17 beta benzoate and estradiol-17 beta cypionate--a preliminary study.

Plasma estradiol-17 beta concentrations were investigated in cows during induced estrus and after an intramuscular injection of 10 mg of estradiol-17 beta benzoate and estradiol-17 beta cypionate to determine a withdrawal period for both preparations. After the estradiol-17 beta benzoate injection, the plasma estradiol-17 beta concentration was higher than the physiological maximum of 24 pg/ml obtained during induced estrus for a period of 114 +/- 10 h (mean +/- SEM). For estradiol-17 beta cypionate the corresponding value was 170 +/- 17 h (mean +/- SEM). A withdrawal period of 7 days for the benzoate ester and of 10 days for estradiol-17 beta cypionate is therefore proposed. These results were confirmed by biopsies taken at the injection site 8 and 15 days after the injection of estradiol-17 beta benzoate and estradiol-17 beta cypionate, respectively. In these biopsies no residues of estradiol-17 beta nor of its esters could be detected.

Animals↗
PubMed1981

16 Alpha-[125I]-beta-estradiol compared with [3H]-beta-estradiol as the tracer in estradiol receptor assays.

We assessed the potential usefulness of 16 alpha-[125I]-beta-estradiol in estradiol receptor assays as compared with a long-used [3H]-beta-estradiol dextran-coated charcoal method, measuring 472 consecutive human breast-cancer cytosols by both procedures. Six different preparations of 16 alpha-[125I]-beta-estradiol were used. Nonspecific binding in five batches was similar and comparable to [3H]-beta-estradiol. Although the sixth batch had increased nonspecific binding, this did not affect results. Dissociation constants were virtually identical (r = 0.94). Results were concordant for 98.5% of cytosols: 161 were negative and 304 positive by both methods and seven were positive by one method, negative by the other. Four were positive with the 125I procedure and undetectable with [3H]-beta-estradiol. Three were measurable by both methods, but were above the cut-off value in one and below it in the other. We find 16 alpha-[125I]-beta-estradiol to be an adequate substitute for [3H]-beta-estradiol in estradiol receptor assays.

Breast Neoplasms↗
PubMed2001

[Cross-over comparison of the pharmacokinetics of estradiol during hormone replacement therapy with estradiol valerate or micronized estradiol].

OBJECTIVE: The aim of this randomized cross-over study was the comparison between a sequential 28-day hormone replacement therapy (HRT) using micronized estradiol and a cyclic 21-day HRT using estradiol valerate with regard to the pharmacokinetics of estradiol. - MATERIAL AND METHODS: Fifty postmenopausal women were randomly assigned to be treated either with Trisequens(R) for 28 days or with Sisare(R) for 21 days. After a wash-out cycle, the women were treated for one cycle with the other preparation in a cross-over fashion. The pharmacokinetic profile of the serum concentrations of estradiol was measured on day 1, 21 and 28 each immediately before and 1, 2, 4, 6, 8, and 10 hours after intake of a tablet, and the AUC (area under the curve) was calculated. - RESULTS: The serum concentrations of estradiol increased from a mean of 10 pg/ml up to 40 pg/ml (Trisequens(R)) and 30 pg/ml (Sisare(R)) on day 1, and to 80 pg/ml (Trisequens(R)) and 60 pg/ml (Sisare(R)) on day 21, and declined to 40 pg/ml (Trisequens(R)) and 10 pg/ml (Sisare(R)) on day 28. The AUC as calculated from both treatment cycles, was significantly higher on day 1, 21, and 28 during treatment with Trisequens(R) than with Sisare(R). This difference was, however, not signifcant on day 1 and 21 of the first treatment cycle. - CONCLUSION: During treatment with 2 mg micronized estradiol the serum concentrations are significantly higher than with 2 mg estradiol valerate. On day 28 of treatment with Sisare(R), the estradiol levels decline to baseline values, while using Trisequens(R) they remain in the range of those measured on day 1.

Aged↗
PubMed1998

2-Hydroxy-4-glutathion-S-yl-17beta-estradiol and 2-hydroxy-1-glutathion-S-yl-17beta-estradiol produce oxidative stress and renal toxicity in an animal model of 17beta-estradiol-mediated nephrocarcinogenicity.

Chronic exposure of male Syrian hamsters to a variety of estrogens has been linked with a high incidence of renal carcinoma. The basis of this species and tissue specificity remains to be resolved. We have recently shown that (i) 17beta-estradiol is nephrotoxic in the hamster in a manner dependent upon the activity of gamma-glutamyl transpeptidase and (ii) 17beta-estradiol is metabolized to a variety of catechol estrogen glutathione conjugates (Butterworth et al., Carcinogenesis, 18, 561-567, 1997). We report that the catechol estrogen glutathione conjugates exhibit redox properties similar to those of the catechol estrogens, and maintain the ability to generate superoxide radicals. Administration of 2-hydroxy-4-glutathion-S-yl-17beta-estradiol or 2-hydroxy-1-glutathion-S-yl-17beta-estradiol (0.27-5.0 micromol/kg) to Syrian hamsters, produces mild nephrotoxicity. Repeated daily administration of 2-hydroxy-4-glutathion-S-yl-17beta-estradiol causes a sustained elevation in urinary markers of renal damage and in the concentration of renal protein carbonyls and lipid hydroperoxides. Catechol estrogen oxidation and conjugation of glutathione in the liver, followed by the selective uptake of the redox active conjugates in tissues rich in gamma-glutamyl transpeptidase may contribute to 17beta-estradiol-induced renal tumors in the hamster.

Animals↗
PubMed1997

Comparative serum estradiol profiles from a new once-a-week transdermal estradiol patch and a twice-a-week transdermal estradiol patch.

Two identical open-label, randomized crossover studies were conducted to compare serum estradiol profiles from the new 12.5- and 25-cm2 once-a-week adhesive patches with those from the 10- and 20-cm2 commercially available twice-a-week Estraderm patches when applied as directed during a 1-week patch-wear period. Both studies were conducted in healthy postmenopausal women; serum estradiol levels were determined by gas chromatography/mass spectroscopy (GC/MS). Although both sizes of both patch treatments produced mean serum estradiol levels in the therapeutic range, the once-a-week patch provided more constant mean levels, avoiding large peak-to-trough fluctuations. As expected, the differences in mean serum estradiol concentrations between the two patch treatments occurred during the second application of the twice-a-week patch. Based on these results, the once-a-week drug in adhesive patch appears to be an acceptable means of hormone replacement therapy.

Administration, Cutaneous↗
PubMed1986

Properties of the estrogen receptors contained in the MtTF4 tumor whose growth is inhibited by estradiol: 17 beta-estradiol, 17 alpha-estradiol and DNA bindings.

The steroid and the DNA bindings of the estrogen receptor of the MtTF4 tumor whose growth is inhibited by estradiol where characterized and compared to those of uterine estrogen receptors. In the tumor cytosol: E protects its binding sites against thermal denaturation, depending on the effects of sodium molybdate upon the dissociation rate of [3H]E at 20 degrees C and the ability of receptor to bind to DNA, the activation (or transformation) process, supposed to be necessary for the full action of estrogen ligand, occurs on estrogen receptor complexes and the calf thymus DNA interacts with estrogen receptor with an affinity similar to that of uterine estrogen receptor. Kinetic and equilibrium studies with 17 alpha-[3H]E both in uterus and tumor indicate that this ligand is fast-associating, fast-dissociating and that its affinity for ER is 2- to 4-fold lower than that of 17 beta-[3H]estradiol one. Competition experiments between 17 beta-[3H]estradiol and the unlabelled 17 alpha epimer reveal, in both uterus and tumor, a time-dependent decrease of the apparent potency of 17 alpha-E to inhibit the binding of [3H]E. It is concluded that the estrogen receptors are very similar in MtTF4 tumor and uterus and the diversity of the response of cell growth to E is due rather to differences at the post-receptor level.

Animals↗
PubMed1989

A rapid, sensitive method for the simultaneous quantitation of estradiol and estradiol conjugates in a variety of tissues: assay development and evaluation of the distribution of a brain-enhanced estradiol-chemical delivery system.

A rapid and sensitive method that permits the simultaneous quantitation of estradiol (E2) and the E2 conjugate [estradiol 17-(1,4-dihydrotrigonellinate)] in biological tissues from rats is described. This method development was necessitated by the design of this E2-chemical delivery system (E2-CDS) which permits the predictable metabolism of the E2-CDS to a charged quaternary ion (E2-Q+) and its subsequent hydrolysis to slowly liberate E2. Based upon in vitro determinations of the rates of oxidation of E2-CDS to E2-Q+ and hydrolysis of E2-Q+ to E2, we anticipated that concentrations of E2-Q+ would be several orders of magnitude higher in tissues than E2. Three steps were used to extract and prepare samples for the radioimmunoassay (RIA) of estradiol. The first step is homogenization and extraction of the biological samples with an organic solvent; the second step is the base catalyzed hydrolysis of the E2 conjugate in 1 N NaOH; and the third step utilizes solid-phase extraction (SPE) with C18 reversed-phase columns which provide a means of achieving a rapid and precise extraction and separation of E2. The analysis of plasma samples does not require the initial solvent extraction. All purified E2 samples were then reconstituted in the assay buffer and assayed by RIA for E2. The application of this procedure to the determination of E2-Q+ and E2 in biological materials was assessed for specificity, reliability and recovery in vitro by using tissues and plasma from rats and in vivo evaluations of the distribution of E2 and E2-Q+ were done using rats treated with 1 mg E2-CDS/kg. Our in vitro analyses revealed that E2 and E2-Q+ could be differentially extracted with a high recovery and that both compounds could be specifically and reliably assayed in brain, plasma, anterior pituitary, liver, kidney, lung, heart and adipose tissue. In vivo analyses revealed that following a single i.v. injection of E2-CDS, brain levels of E2 exceeded serum levels by 30-, 41-, and 82-fold while brain levels of E2-Q+ exceeded serum levels by 33-, 70-, and 294-fold at 1, 7 and 14 days, respectively. Collectively, these data indicate that E2-Q+ and E2 can be reliably quantitated in a variety of tissues following the administration of an E2-chemical delivery system.

Animals↗
PubMed1980

Subdermal estradiol pellets following hysterectomy and oophorectomy. Effect upon serum estrone, estradiol, luteinizing hormone, follicle-stimulating hormone, corticosteroid binding globulin-binding capacity, testosterone-estradiol binding globulin-binding capacity, lipids, and hot flushes.

Subderman estradiol (E2) pellets (25 mg) were inserted immediately after hysterectomy and oophorectomy in 22 menstruating women, ages 29 to 50 years. Serum samples were obtained daily for 7 days, weekly for 4 weeks, and at monthly intervals for 6 months. Although there was significant variation between patients, E2 levels remained within the follicular phase range, averaging 50 to 70 pg/ml for 3 months, and then slowly declining to a mean of 37 pg/ml at 6 months, when new pellets were inserted. Over the entire study period, the E2:estrone (E1) ratio was greater than unity. Subdermal E2 pellets limited the rise in luteinzing hormone (LH) and follicle-stimulating hormone (FSH) after gonadectomy and the levels of LH and FSH 6 months after the insertion of E2 pellets were significantly lower (p < 0.01) than in 20 postmenopausal women who had undergone oophorectomy and whose serum E2 levels were less than 20 pg/ml. Serum corticosteroid binding globulin-binding capacity (CBG-BC) and serum testosterone-estradiol binding globulin-binding capacity (TeBG-BC) remained unchanged with E2 pellets. Although high-density lipoprotein-cholesterol increased significantly (p < 0.05), low-density lipoprotein-cholesterol, total cholesterol, and triglycerides were unaffected, except for a rise in triglycerides in three older women with diabetes mellitus and hypertension. There were no complaints of severe hot flushes. Women who had vasomotor symptaoms had mild or moderate flushes that occurred at 5 or 6 months after replacements of the pellets. Thus, E2 pellets are an effective form of parenteral estrogen replacement therapy and offer both practical and theorteical advantages over other forms of estrogen.

Adult↗
PubMed1986

Total estradiol, free estradiol, sex hormone-binding globulin, and the fraction of estradiol bound to sex hormone-binding globulin in human follicular fluid.

Sex hormone-binding globulin (SHBG), percent free estradiol (E2), the fraction of E2 bound to SHBG, and total E2 were measured in the serum and follicular fluid of 12 women (25 follicles) who had received gonadotropin stimulation in an in vitro fertilization program. The women were classified as high or low responders based on peak serum E2 levels (high responders: peak E2, greater than 1500 pg/ml; low responders: peak E2, less than 1000 pg/ml). During treatment, serum levels of SHBG increased in high responders from 55 +/- 8.8 (+/- SEM) to 96 +/- 16 nM (P less than 0.01), but did not change in low responders. SHBG was more concentrated in follicular fluids from high responders (142 +/- 12.5 nM) than in those from low responders (44.4 +/- 5.8 nM). A positive correlation was found between serum and follicular fluid levels of SHBG (r = 0.873; P less than 0.01). In follicular fluid, total E2 levels, which varied from 100-2650 ng/ml, correlated (r = 0.790; P less than 0.01) closely with SHBG levels. The percent free E2 averaged 5.9% (range, 4-10.6%) in follicular fluid compared to 1.8% (range, 1.5-2.1%) in serum. An inverse correlation (r = -0.661; P less than 0.01) was found between total E2 concentrations and percent free E2 in follicular fluid. The relationship between serum and follicular fluid levels of SHBG suggests that SHBG in follicles arises from the circulation. Although SHBG is present in follicular fluid in amounts similar to those in serum, the large quantities of E2 in preovulatory follicules exceed the binding capacity for SHBG, and the majority of E2 appears to be bound to albumin. Hence, it seems unlikely that SHBG in follicular fluid regulates estrogen action in ovarian target cells.

Adult↗
PubMed2005

Sulfotransferase 2A1 forms estradiol-17-sulfate and celecoxib switches the dominant product from estradiol-3-sulfate to estradiol-17-sulfate.

Using recombinant sulfotransferases (SULTs) expressed in E. coli, beta-estradiol (E2) sulfonation was examined to determine which SULT enzyme is responsible for producing E2-17-sulfate (E2-17-S). SULTs 1A1*1, 1A1*2, 1A3, 1E1 and 2A1 all sulfated E2 to varying extents. No activity was observed with SULT1B1. Among the SULTs studied, SULT2A1 produced primarily E2-3-sulfate (E2-3-S), but also some E2-17-S and trace amounts of E2 disulfate. SULT2A1 had a K(m) value of 1.52 microM for formation of E2-3-S and 2.95 microM for formation of E2-17-S. SULT2A1 had the highest V(max) of 493 pmol/min/mg protein for formation of E2-3-S, which was 8.8- and 47-fold higher than the maximal rates of formation of E2-17-S and E2 disulfate, respectively. SULT2A1 formed E2-3-S more efficiently. However, when celecoxib (0-160 microM) was included in the incubation with either SULT2A1 or human liver cytosol, sulfonation switched from E2-3-S to E2-17-S in a concentration-dependent manner. The ratio of E2-17-S/E2-3-S went up to 15 with SULT2A1, and was saturated at 1 with human liver cytosol. In both cases, more E2-17-S was formed, with the unreacted E2 remained unchanged, suggesting celecoxib probably bound to a separate effector site to cause a conformational change in SULT2A1, which favored production of E2-17-S. The ability of celecoxib to alter the position of sulfonation of E2 may in part explain its success in the experimental prevention and treatment of breast cancer.

Celecoxib↗
PubMed1999

Cycle control with oral contraceptives containing 20 micrograms of ethinyl estradiol. A multicenter, randomized comparison of levonorgestrel/ethinyl estradiol (100 micrograms/20 micrograms) and norethindrone/ethinyl estradiol (1000 micrograms/20 micrograms).

A randomized, open-label, multicenter study was undertaken to compare the effects of oral contraceptives (OC) containing 100 micrograms levonorgestrel (LNG)/20 micrograms ethinyl estradiol (EE) (Aless/Loette) and 1000 micrograms norethindrone acetate (NETA)/20 micrograms EE (Loestrin Fe 1/20) on menstrual cycle control over four cycles of use. A total of 84 evaluable women provided 274 cycles of exposure in the LNG/EE group, and 89 women provided 289 cycles of exposure in the NETA/EE group. Overall, the LNG/EE group achieved a consistently higher percentage of normal menstrual cycles as well as a lower rate of intermenstrual bleeding and amenorrhea than the NETA/EE group. In cycle 4, 63.8% of cycles were normal in the LNG/EE group compared with 41.9% in the NETA/EE group (p < 0.005). Of the total cycles in the NETA/EE group, 10% were amenorrheic, compared with 1.1% in the LNG/EE group. The occurrence of bleeding and/or spotting was significantly lower in cycles 2 and 3 in the LNG/EE group (41.7% and 34.8%, respectively) compared with the NETA/EE group (62.3% and 56.3%; p < 0.05). Other cycle variables were generally similar between groups, as was the incidence of adverse events. These results demonstrate that good cycle control was achieved with an OC containing 20 micrograms EE and that 100 micrograms LNG/20 micrograms EE produces better cycle control than 1000 micrograms NETA/20 micrograms EE.

Contraceptives, Oral, Hormonal↗
PubMed1985

Interaction of estradiol and estriol with uterine estrogen receptor in vivo and in excised uteri or cell suspensions at 37 C: noncooperative estradiol binding and absence of estriol inhibition of estradiol-induced receptor activation and transformation.

The partial agonist and antagonist properties of estriol (E3) have been related to the brief nuclear retention of receptor-E3 complexes and to the lower affinity of E3 for the receptor compared to estradiol (E2). More recently, it was proposed that the partial agonist/antagonist activity of E3 may be due to its ability to eliminate positive cooperative binding of [3H]E2 to cytosolic estrogen receptor. In this model, positive cooperativity is related to receptor activation and transformation. We first examined the long term effects of E3 on E2 action in vivo. Mature ovariectomized rats were treated for 16 days with E2, E3, or mixtures of these two substances delivered through Alzet pumps at a constant hourly rate (E2, 0.04 microgram; E3, 0.4 and 0.04 microgram; E2 and E3, 0.04 and 0.4 microgram). The effects of E3 on uterine growth, induction of progesterone receptor synthesis, and activation (nuclear binding) of estrogen receptor suggest that when given continuously, E3 acts as a full agonist and does not inhibit E2 action. Furthermore, incubation of uteri at 37 C with [3H]E2 in the presence of a 1- to 20-fold molar excess of nonradioactive E3 did not alter the subcellular distribution of receptor-[3H]E2 complexes (80% nuclear and 20% cytosolic), demonstrating that E3 does not inhibit E2-induced receptor activation (i.e. the increased nuclear binding of receptor). Similarly, 4S to 5S transformation of [3H]E2-labeled estrogen receptor in intact uteri was not inhibited by E3. Equilibrium binding of [3H]E2 to uterine cell suspensions at physiological temperature (37 C) was noncooperative; nonradioactive E3 did not alter the affinity of the estrogen receptor for [3H]E2; Dixon plot analysis indicates that E3 is a purely competitive inhibitor of [3H]E2 binding. This, in conjunction with the lower affinity of the receptor for E3 than for E2, adequately explains the agonistic-antagonistic properties of E3.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

The effects of plasma estradiol levels on increases in vertebral and femoral bone density following therapy with estradiol and estradiol with testosterone implants.

Percutaneous estradiol (E2) implants effectively preserve bone density in postmenopausal women. However, these implants are often given with testosterone, which may itself have an anabolic effect on bone. To determine whether testosterone confers any additional bone-sparing effect, we studied 50 postmenopausal women randomly allocated to receive E2 (75 mg) alone or with testosterone (100 mg) every 6 months for 1 year. Women with an intact uterus received cyclic norethindrone (5 mg) for 10 days of each calendar month. Twenty-five untreated women were recruited to act as a reference group. Bone density was measured at the lumbar spine and proximal femur by dual x-ray densitometry. By 1 year, bone density at the lumbar spine had fallen by 1.8% in the reference group. In the women treated with E2 alone, it increased significantly by 7.8% (P less than .0001) and in those receiving E2 with testosterone, it increased by 6.3% (P less than .0001). At the femoral neck, bone density decreased by 3% in the controls and increased by approximately 4% in both treated groups (P less than .0001). The increase in bone density at these sites was unrelated to the woman's chronological age, menopausal age, or initial bone density. However, it correlated significantly with the serum E2 levels attained after 1 year of therapy. In no treated patients did bone density decrease significantly. These data show that testosterone confers no additional bone-sparing effect in postmenopausal women.

Bone Density↗