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At least 235 records · Page 13Linked to original sources

PubMed2002

Effects of estradiol and estradiol sulfamate on the liver of ovariectomized or ovariectomized and hypophysectomized rats.

This study was performed to evaluate and compare the effects of estradiol sulfamate (J995) and estradiol (E2) on the hepatic levels of the estrogen receptor (ER) and its mRNA, in ovariectomized (OVX) and OVX+hypophysectomized (OVXHX) female rats and to study the effects on the liver-derived serum compounds angiotensin I, triglycerides, high-density lipoprotein (HDL) and cholesterol. ER concentrations were determined using ligand-binding assay (LBA) and enzyme immuno assay (EIA), and the mRNA levels using solution hybridization. The rats were treated orally (p.o.) or subcutaneously (s.c.) for 7 days, with treatments initiated 14 days after surgery. No differences were found in ER mRNA levels between J995 and E2 treated rats. The s.c. administered estrogens increased ER levels in OVX rats. Addition of GH+DEX to OVXHX rats restored the ER to levels above those seen in intact rats, whereas simultaneous oral treatment with E2 significantly decreased ER levels again. The s.c. treatment with either J995 or E2 limited the increase caused by addition of GH+DEX. After oral treatment angiotensin I levels were increased by E2, but not by J995, while triglycerides, HDL and cholesterol levels were decreased by oral E2, J995 showing a similar pattern but was less effective. In summary, these results on hepatic ER levels and estrogen dependent compounds produced by the liver showed that J995 has a lower impact on the normal liver functions after oral treatment than E2. Thus, J995 is a very promising substance for development of oral estrogen treatment with reduced hepatic side effects.

Angiotensin I↗

PubMed1998

Estradiol-mimetic probes. Preparation of 17 alpha-(6-aminohexynyl)estradiol biotin, fluorescein and acridinium conjugates.

3-O-tert-Butyldimethylsilyl-17 alpha-(6-mesyloxyhexynyl)estradiol was converted to the azide in 60-70% yield with NaN3/DMPU, then reduced to the corresponding amine (> 95% yield). Acylation with the N-hydroxysuccinimide esters of biotin, 5-carboxyfluorescein and 10-(3-sulfopropyl)-N-tosyl-N-(3- carboxypropyl)acridinium-9-carboxamide gave the title conjugates. The KDs of the tracers with an estradiol antibody ranged from 97-197 nM.

Acridines↗

PubMed2006

The greater reactivity of estradiol-3,4-quinone vs estradiol-2,3-quinone with DNA in the formation of depurinating adducts: implications for tumor-initiating activity.

Strong evidence supports the idea that specific metabolites of estrogens, mainly catechol estrogen-3,4-quinones, can react with DNA to become endogenous initiators of breast, prostate, and other human cancers. Oxidation of the catechol estrogen metabolites 4-hydroxyestradiol (4-OHE2) and 2-OHE2 leads to the quinones, estradiol-3,4-quinone (E2-3,4-Q) and estradiol-2,3-quinone (E2-2,3-Q), respectively. The reaction of E2-3,4-Q with DNA affords predominantly the depurinating adducts 4-OHE2-1-N3Ade and 4-OHE2-1-N7Gua, whereas the reaction of E2-2,3-Q with DNA yields the newly synthesized depurinating adduct 2-OHE2-6-N3Ade. The N3Ade adducts are lost from DNA by rapid depurination, while the N7Gua adduct is lost from DNA with a half-life of approximately 3 h at 37 degrees C. To compare the relative reactivity of E2-3,4-Q and E2-2,3-Q, the compounds were reacted individually with DNA for 0.5-20 h at 37 degrees C, as well as in mixtures (3:1, 1:1, 1:3, and 5:95) for 10 h at 37 degrees C. Depurinating and stable adducts were analyzed. In similar experiments, the relative reactivity of 4-OHE2 and 2-OHE2 with DNA was determined after activation by lactoperoxidase, tyrosinase, prostaglandin H synthase (PHS), or 3-methylcholanthrene-induced rat liver microsomes. Starting with the quinones, the levels of depurinating adducts formed from E2-3,4-Q were much higher than that of the depurinating adduct from E2-2,3-Q. Similar results were obtained with lactoperoxidase or tyrosinase-catalyzed oxidation of 4-OHE2 and 2-OHE2, whereas with activation by PHS or microsomes, a relatively higher amount of the depurinating adduct from E2-2,3-Q was detected. These results demonstrate that the E2-3,4-Q is much more reactive with DNA than E2-2,3-Q. The relative reactivities of E2-3,4-Q and E2-2,3-Q to form depurinating adducts correlate with the carcinogenicity, mutagenicity, and cell-transforming activity of their precursors, the catechol estrogens 4-OHE2 and 2-OHE2. This is essential information for understanding the cancer risk posed by oxidation of the two catechol estrogens.

Adenine↗

PubMed1986

Effect of estradiol-17 beta and luteinizing hormone on progesterone secretion by luteal cells from early pregnant, estradiol benzoate-treated and human chorionic gonadotropin-treated sows.

The present study was conducted to examine the effect of estradiol 17 beta (E2) and luteinizing hormone (LH) on progesterone (P4) secretion by luteal cells from early pregnant, estradiol benzoate (EB)-treated and hCG-treated sows and to compare the sensitivity of these cells to used exogenous hormones in vitro. Trypsin-dispersed luteal cells (5 X 10(4) cells/ml) were incubated with E2 (doses: 0.001, 0.01, 0.1, 1 and 5 micrograms/ml), with LH (doses: 0.01, 0.1 and 1 microgram/ml) and with E2 (1 microgram) plus LH (0.01, 0.1 and 1 microgram doses). Control cultures were incubated without exogenous hormones. The P4 level was estimated by radioimmunoassay after 1, 3 and 6 hour incubation. Luteal cells from hCG-treated sows released significantly more (P less than 0.05) P4 than the cells from EB-treated and pregnant pigs, the luteal cells from pregnant sows produced the least P4 amounts (P less than 0.05). The cells from pregnant pigs enhanced P4 secretion under influence of higher doses of LH and the cells from EB-treated sows under lower LH doses. The cells from hCG-treated animals did not respond to LH. E2 did not change P4 production by luteal cells from sows in the three investigated physiological stages, only the 0.01 microgram E2 dose stimulated (P less than 0.05) P4 release by the cells from pregnant pigs. E2 inhibited luteotropic LH action upon P4 secretion by luteal cells from pregnant and EB-treated sows. The results suggest that the luteal cells from early pregnant, EB-treated and hCG-treated sows differ from each other in steroidogenic potency and in the strength of reaction to E2 and LH.

Animals↗

PubMed2001

Crystal structure of a recombinant anti-estradiol Fab fragment in complex with 17beta -estradiol.

The crystal structure of a Fab fragment of an anti-17beta-estradiol antibody 57-2 was determined in the absence and presence of the steroid ligand, 17beta-estradiol (E2), at 2.5 and 2.15-A resolutions, respectively. The antibody binds the steroid in a deep hydrophobic pocket formed at the interface between the variable domains. No major structural rearrangements take place upon ligand binding; however, a large part of the heavy chain variable domain near the binding pocket is unusually flexible and is partly stabilized when the steroid is bound. The nonpolar steroid skeleton of E2 is recognized by a number of hydrophobic interactions, whereas the two hydroxyl groups of E2 are hydrogen-bonded to the protein. Especially, the 17-hydroxyl group of E2 is recognized by an intricate hydrogen bonding network in which the 17-hydroxyl itself forms a rare four-center hydrogen bond with three polar amino acids; this hydrogen bonding arrangement accounts for the low cross-reactivity of the antibody with other estrogens such as estrone. The CDRH3 loop plays a prominent role in ligand binding. All the complementarity-determining regions of the light chain make direct contacts with the steroid, even CDRL2, which is rarely directly involved in the binding of haptens.

Amino Acid Sequence↗

PubMed2005

A study of the control of climacteric symptoms in postmenopausal women following sequential regimens of 1 mg 17beta-estradiol and trimegestone compared with a regimen containing 1 mg estradiol valerate and norethisterone over a two-year period.

OBJECTIVE: To compare the efficacy of two sequential 17beta-estradiol (17beta-E2)/trimegestone (TMG) combinations with the sequential estradiol valerate (E2V)/norethisterone (NET) regimen in relieving climacteric symptoms. STUDY DESIGN: This was a double-blind, randomized, multicenter study conducted among 1218 Caucasian (99%) postmenopausal women with an intact uterus in seven European countries and Israel, over 13 cycles (each of 28 days). Study duration was extended further for 13 cycles, with 531 women receiving treatment for up to 26 cycles. Treatments consisted of 1 mg 17beta-E2 on days 1-14 and 1 mg 17beta-E2/0.125 mg TMG or 0.25 mg TMG on days 15-28, and 1 mg E2V on days 1-16 and 1 mg E2V/1 mg NET on days 17-28. RESULTS: Rapid and significant reductions in the mean daily number and severity of hot flushes and in the mean daily number of nocturnal sweats were established in most women with 1 mg 17beta-E2/0.25 mg TMG and E2V/NET. These treatments also induced a significant improvement in the quality-of-life assessments. CONCLUSION: The 1 mg 17beta-E2/0.25 mg TMG regimen provides rapid and effective relief of menopausal symptoms, with a reduction in the number of hot flushes "at least as good as" that of the E2V/NET comparator.

Administration, Oral↗

PubMed2005

Efficacy on climacteric symptoms of a continuous combined regimen of 1 mg 17beta-estradiol and trimegestone versus two regimens combining 1 or 2 mg 17beta-estradiol and norethisterone acetate.

OBJECTIVES: To compare the efficacy of a continuous combined regimen of 1mg 17beta-estradiol (17beta-E2) and 0.125 mg trimegestone (TMG) with two continuous combined 17beta-E2/norethisterone acetate (NETA) combinations in the relief of climacteric symptoms in postmenopausal women. STUDY DESIGN: This was a randomized, double-blind, multicenter study conducted in 13 countries over a 2-year period. Healthy postmenopausal women with an intact uterus were treated with 1 mg 17beta-E2/0.125 mg TMG, 2 mg 17beta-E2/1 mg NETA or 1 mg 17beta-E2/0.5 mg NETA for up to 26 cycles, each of 28 days. RESULTS: The 1 mg 17beta-E2/0.125 mg TMG combination was effective in significantly reducing the mean daily number and severity of hot flushes and in reducing the number of night sweats from cycle 1 onward. No overall significant differences between this regimen and the comparators were detected. Other efficacy variables, including the Kupperman index, psychofunctional disorders and quality-of-life sub-scales, experienced a similar improvement from baseline with all treatments. CONCLUSION: Continuous combined 1 mg 17beta-E2/0.125 mg TMG provides relief of menopausal symptoms that is non-inferior to both 17beta-E2/NETA combinations. Furthermore, trimegestone appeared to provide a better improvement of depressive mood than 0.5 mg NETA when combined with 1 mg 17beta-estradiol.

Administration, Oral↗

PubMed2005

A comparative 2-year study of the effects of sequential regimens of 1 mg 17beta-estradiol and trimegestone with a regimen containing estradiol valerate and norethisterone on the bleeding profile and endometrial safety in postmenopausal women.

OBJECTIVE: To compare the bleeding profiles and endometrial protection of two sequential regimens of 17beta-estradiol (17beta-E2) and trimegestone (TMG) with a sequential estradiol valerate (E2V)/norethisterone (NET) regimen. STUDY DESIGN: This was a randomized, double-blind, multicenter study conducted in eight countries in healthy, postmenopausal women with an intact uterus. A total of 1218 women were enrolled into the initial 1-year study (13 cycles), and subsequently 531 of these received treatment for a further year (26 cycles). Treatment regimens were 1 mg 17beta-E2 on days 1-14 and 1 mg 17beta-E2/0.125 mg TMG or 1 mg 17beta-E2/0.25 mg TMG on days 15-28, and 1 mg E2V on days 1-16 and 1 mg E2V/1 mg NET on days 17-28. RESULTS: Mean percentage of women reporting onset of withdrawal bleeding episodes during the week following discontinuation of progestogen was higher in the 1 mg 17beta-E2/0.25 mg TMG group than in the other two treatments, showing a more efficient progestogen effect on the endometrium and good predictability of bleeding onset with this treatment. The mean numbers and average lengths of bleeding episodes were similar in the three treatment groups. Overall, the bleeding profile was more favorable with 1 mg 17beta-E2/0.25 mg TMG than with the lower-dose TMG preparation. Both of the TMG regimens demonstrated a good protective effect on endometrial proliferation, with the 0.25 mg TMG dose showing a lower incidence of proliferative endometrium. CONCLUSION: The 1 mg 17beta-E2/0.25 mg TMG regimen showed an adequate protection of the endometrium, with an overall favorable bleeding profile.

Administration, Oral↗

PubMed2001

Serum concentrations of 17beta-estradiol and estrone after multiple-dose administration of percutaneous estradiol gel in symptomatic menopausal women.

In two multicenter phase III efficacy studies, blood samples were obtained to evaluate the serum concentrations of 17beta-estradiol (E2) and unconjugated estrone (E1) after administration of a percutaneous gel or transdermal patch containing estradiol. In postmenopausal women, normal laboratory E2 and E1 serum concentrations range from 10-30 pg/mL and 20-40 pg/mL, respectively. Study subjects were healthy postmenopausal women with moderate to severe hot flushes occurring at least seven times daily or 60 times per week. Study 1 was a randomized, double-blind, multicenter study of percutaneous E2 gel 1.25 or 2.5 g (0.75 and 1.5 mg E2, respectively) versus placebo gel. Study 2 was a double-blind (blinded to E2 gel dose), randomized, active-controlled, multicenter, 12-week phase 3 study of E2 gel 0.625, 1.25, or 2.5 g (0.375, 0.75, or 1.5 mg E2, respectively) versus a transdermal E2 patch delivering 0.05 mg E2 per day. Serum E2 and E1 concentrations were evaluated at baseline and at week 12 for study 1 and at baseline and weeks 4, 8, and 12 for study 2 using radioimmunoassay. Median serum concentrations of E2 after 1.25- and 2.5-g gel administration appeared to be dose-proportional throughout both studies. In study 1, the median serum concentrations of E2 at week 12 were 33.5 and 65.0 pg/mL for 1.25- and 2.5-g gel dose, respectively. The corresponding E1 values were 49.0 and 58.0 pg/mL. In study 2, both E2 and E1 concentrations were relatively stable at weeks 4, 8, and 12. E2 values at week 12 for 0.625-, 1.25-, and 2.5-g gel doses and E2 patch were 25.0, 32.0, 60.0, and 38.5 pg/mL, respectively. The corresponding E1 values were 39.0, 41.0, 62.5, and 40.0 pg/mL. Application of the 1.25-g gel dose and a transdermal patch delivering 50 microg per day of E2 resulted in comparable median E2 and E1 concentrations. However, the 0.625-g gel dose did not produce E2 levels in a range expected to be consistently therapeutic in most postmenopausal women.

Administration, Topical↗

PubMed2004

Cytochrome P450-mediated oxidation of glucuronide derivatives: example of estradiol-17beta-glucuronide oxidation to 2-hydroxy-estradiol-17beta-glucuronide by CYP 2C8.

In the classical metabolic oxidation scheme, hydrophobic endogenous or xenobiotic compounds undergo phase I oxidation, generally catalyzed in the liver by cytochromes P450, followed by phase II conjugation reactions, in a way that allows much more polar metabolites to be expelled from the cell through active transport mechanisms. Cytochrome P450-mediated oxidation of steroid sulfate has been described, suggesting that oxidation of polar metabolites such as glucuronide derivatives of endogenous compounds can occur. As an example, we report here that hydroxyestradiol-17beta-glucuronide can be directly formed through oxidation of estradiol-17beta-glucuronide on the aromatic C2 position. This reaction is specifically catalyzed by CYP 2C8, which is more active in female than in male human liver microsomes. A thorough docking of the molecule within the CYP 2C8 crystal structure shows that the active site is large enough to handle a glucuronide conjugate. Moreover, the most energetically favored position of the bound ligand is fully consistent with the recently published structural determinants of substrate specificity of the CYP 2C8 active site. This is the first demonstration of cytochrome P450-mediated oxidation of a steroid glucuro-conjugate. Such oxidation of a glucuronide should be a general process since, in addition to estradiol and testosterone glucuronide, it has been observed for xenobiotic compounds, e.g., diclofenac or naproxen glucuronide.

Animals↗

PubMed1975

Identification of radioactive 17beta-estradiol-17-beta-D-glucuronide and 17alpha-estradiol-17-beta-D-glucuronide in the urine of the domestic fowl after intramuscular injection of [4-14C]estrone.

Two previously uncharacterized radioactive estrogen conjugates, 17beta-estradiol-17-beta-D-glucuronide (3-hydroxyestra-1,3,5(10)-trien-17beta-D-glucopyranosiduronate) and 17alpha-estradiol-17beta-D-glucuronide (3-hydroxyestra-1,3,5(10)-trien-17alpha-yl-beta-D-glucopyranosiduronate), have been identified in small but significant amounts in avian urine and in a ratio of approximately 2:1 after intramuscular injection of [4-14C]estrone.

Animals↗

PubMed1979

Relative binding of testosterone and estradiol to testosterone-estradiol-binding globulin.

The binding of estradiol (E2) and testosterone (T) to testosterone-estradiol-binding globulin (TeBG) was studied in vivo at 37 C by three independent methods: equilibrium dialysis, steady state polyacrylamide gel electrophoresis, and TeBG-ligand dissociation kinetics. Equilibrium dialysis was performed at 37 C with the dialysate containing human serum albumin in amounts equivalent to that of the plasma dialysand. Scatchard analysis indicated that under these conditions E2 does not measurably bind to TeBG, while T has a Kd of 3.7 X 10(-10) M. Similarly, Scatchard-type analysis of E2 binding to TeBG in steady state polyacryalmide gel electrophoresis at 37 C revealed no high affinity saturable binding, while dihydrotestosterone was bound with a Kd of 2.7 X 10(-10) M. Examination of the dissociation kinetics of T and E2 ffrom TeBG revealed that the mean (+/-SD) T1/2 of dissociation of T from plasma at 37 C (10.8 +/- 2.4 min) was significantly shortened to 3.5 +/- 0.4 min by saturation of plasma with dihydrotestosterone (P less than 0.01), whereas that of E2 (8.9 +/- 1.4 min) was not changed (9.6 +/- 3.0 min). These data suggest that TeBG is not an important binder of plasma E2 at physiological temperatures and explain the observation that in diseases characterized by high TeBG levels, such as hyperthyroidism and liver disease, the MCR and free E2 levels have generally been normal.

Adult↗

PubMed1998

In vivo properties of the conjugates of mitomycin C with estradiol benzoate and estradiol: pharmacokinetics and antitumor characteristics against P388 leukemia and sarcoma 180.

Conjugates of mitomycin C (MMC) with estradiol benzoate and estradiol via glutaric acid, abbreviated to EB-glu-MMC and E-glu-MMC, respectively, as previously reported, were examined concerning their pharmacokinetic behaviors and antitumor effects against two kinds of general and popular tumors, P388 leukemia and Sarcoma 180. EB-glu-MMC and E-glu-MMC were dissolved in propylene glycol. Their solution was administered intraperitoneally to rats and mice in order to examine their plasma concentration-time profiles and antitumor characteristics, respectively. After the administration of EB-glu-MMC, EB-glu-MMC was detected slightly in blood only in the initial stage, while E-glu-MMC and MMC were observed there for a prolonged period. In the administration of E-glu-MMC, a similar phenomenon was observed but the drug retention effect seemed lower than that in EB-glu-MMC. In the antitumor test against P388 leukemia, E-glu-MMC exhibited a better effect than EB-glu-MMC; however, neither conjugate surpassed the effect of MMC. The toxic side effect was improved in each conjugate. As to the growth inhibition against Sarcoma 180, EB-glu-MMC and E-glu-MMC produced good effect and improved the toxic side effect. Especially, in the administration of EB-glu-MMC at the dose of 30 mg eq MMC/kg, a decrease in tumor volume was observed in the latter stage. EB-glu-MMC and E-glu-MMC were demonstrated to produce prolonged retention, to enter the systemic circulation to a fair extent, and to exhibit a good effect against the general solid tumor, Sarcoma 180, in vivo.

Animals↗

PubMed2002

Antitumor activities of conjugates of mitomycin C with estradiol benzoate and estradiol via glutaric acid in suspension dosage form.

Conjugates of mitomycin C (MMC) with estradiol bezoate and estradiol via glutaric acid (EB-glu-MMC and E-glu-MMC, respectively) were examined for their antitumor activities against P388 leukemia and sarcoma 180. EB-glu-MMC and E-glu-MMC were suspended in 10% (v/v) propylene glycol in saline and administered intraperitoneally to mice bearing P388 leukemia intraperitoneally or to mice bearing sarcoma 180 subcutaneously. The antitumor effect against P388 leukemia was greater in the order MMC>E-glu-MMC>EB-glu-MMC, and only the former two compounds significantly increased life span. On the other hand, EB-glu-MMC and E-glu-MMC showed suppression of sarcoma 180 growth at higher doses close to or better than MMC. In the mixture of 1/15 M phosphate buffer (pH 7.4, ionic strength (mu) adjusted to 0.3 with NaCl)-propylene glycol (9:1, v/v) at 37 degrees C, MMC was released much more slowly from EB-glu-MMC suspension than from E-glu-MMC suspension. With regard to chemotherapy against sarcoma 180, both conjugates were considered to supply MMC slowly but effectively at higher doses.

Animals↗

PubMed2005

Quantitative analysis of 17beta-estradiol in river water by fluorometric enzyme immunoassay using biotinylated estradiol.

A sensitive and simple immunoassay to determine 17beta-estradiol (E2) in fresh water was developed. The method is based on a solid-phase avidin-biotin binding assay and solid phase extraction. The binding event of E2 to the antibody is detected indirectly by the competitive reaction between E2 and biotinylated estradiol (BE) as a tracer for the limited binding sites of antibodies immobilized onto the wall of a microtiter plate. Namely, E2 concentrations are determined from the strong interaction between BE and avidin conjugated with horseradish peroxidase (avidin-HRP). In order to achieve a sensitive measurement for the binding of BE to the antibody immobilized on the microtiter plate substrate, QuantaBlu fluorogenic peroxidase substrate (QFPS) was employed. The detection limit and the linear range of E2 determination were 27 pM and 27 - 7480 pM, respectively. The relative standard deviations (RSD) for the E2 assay were between 0.3 and 12.0% (n = 3). The cross-reactivities of several other estrogens in this assay system were also investigated. No serious influences from any cross-reaction caused by other estrogens tested in this experiment were observed. The determination of E2 in water samples from eight rivers and a marsh in Hokkaido was performed by the immunoassay combined with solid phase extraction. It was found that the concentration of E2 was in the range between 0.06 and 67 pM.

Biotinylation↗

PubMed1992

Effects of exogenous estradiol-17 beta on luteinizing hormone, progesterone, and estradiol-17 beta concentrations before and after prostaglandin F2 alpha-induced termination of pregnancy and pseudopregnancy in gilts.

This study evaluated the influence of exogenous estradiol-17 beta (E2) administration on LH concentrations and the number of animals returning to estrus after the termination of pregnancy or pseudopregnancy in gilts. Gilts were mated (pregnant; n = 11) on the 1st d of estrus or received 5 mg of estradiol valerate i.m. at d 11 to 15 after the onset of estrus (pseudopregnant; n = 9). Gilts were treated with prostaglandin F2 alpha (PGF2 alpha, 15 and 10 mg) at 12-h intervals on d 44 of pregnancy or pseudopregnancy. The day of abortion or luteolysis (progesterone less than .2 ng/mL) was considered d 0. Six pregnant and four pseudopregnant gilts received s.c. an E2 capsule (24 mg of E2) on d -20 and additional E2 capsules on d -13 and -6. The E2 capsules were removed on the day after PGF2 alpha administration. Blood samples were collected at 12-h intervals from d -21 to -3, at 6-h intervals from d -2 to 21 or the onset of estrus, and at 15-min intervals for 8 h on d -2, 1, 4, 7, 10, 14, and 18. After each 8-h sampling period, gilts were treated i.v. with GnRH at .5 micrograms/kg of BW and blood samples collected at 10-min intervals for 3 h. A greater (P less than .05) proportion of sham-treated gilts than of E2-treated gilts exhibited a preovulatory-like LH surge after abortion/luteolysis. It was evident that E2 supplementation before luteolysis reduced the ability of pregnant and pseudopregnant gilts to return to estrus.

Abortion, Induced↗

PubMedDate not supplied

Specific binding of 3H-estradiol to the cytosol of rat pancreas and uterus: bound sites in pancreatic extracts do not translocate 3H-estradiol to nuclei suggesting a basic difference in mode of action.

In parallel sets of experiments, cytosol fractions from rat pancreas and uterus were incubated with 2 nM 3H-estradiol in the presence or absence of nuclei from pancreas and liver. After incubation for 1 hr at room temperature, the nuclei were removed by centrifugation and specific binding determined in the cytosol fractions as well as in the separated nuclei. The protein that binds 3H-estradiol in uterine extracts translocated the hormone to nuclei of pancreas and liver while the one in pancreas was devoid of this activity. It is presumed, therefore, that modification of transcription is not a primary action of the steroid-bound complex in pancreas.

Animals↗

PubMed2000

Treatment of noncyclic lactating dairy cows with progesterone and estradiol or with progesterone, GnRH, prostaglandin F2 alpha, and estradiol.

The efficacy of two programs for treating noncyclic cows was compared. In trial 1, 478 cows in five herds were randomly divided into two groups. Cows in one group (C group) were treated with an intravaginal progesterone device for 8 d followed in 48 h by 1 mg of estradiol benzoate to cows that had not been detected in estrus since device removal. Those in the other group (CGP group) were treated with progesterone and estradiol as for the C group plus 10 micrograms of a GnRH agonist (buserelin) at device insertion and 25 mg of PGF2 alpha 7 d after device insertion. In trial 2 with 729 cows in nine herds, the treatments were similar to those in trial 1 except that the duration of progesterone treatment was 7 d. No significant difference was found between trials and results from both trials were combined. Compared with C group cows, CGP group cows had a greater estrous response rate (93.2 vs. 89.1%), a greater conception rate to first artificial insemination (AI, 47.1 vs. 29.4%), marginally lower conception rate to second AI (52.9 vs. 59.7%), lower nonpregnancy rate (8.3 vs. 11.1%), and shorter intervals from the start of breeding to conception by AI (9.8 vs. 15.3 d) or by AI or natural mating (21.6 vs. 26.3 d). The treatment protocol used for the CGP group achieved better reproductive performance than that used for the C group.

Animals↗