Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:APRD00691 (EE2)
 7,802 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Concentrations of unconjugated dehydroepiandrosterone, estradiol, and estriol were measured in samples of amniotic fluid from uneventful pregnancies of 9-40 weeks conceptual age. There was no apparent influence of fetal sex upon the levels of these steroids. Dehydroepiandrosterone concentrations rose slightly from 9-20 weeks, and then showed little further change. Estradiol concentrations declined slightly from 9-20 weeks; after 32 weeks gestation, there was a 2-fold rise to term. Estriol levels rose in almost exponential fashion throughout gestation.
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PMID:Studies on human sexual development. VI. Concentrations of unconjugated dehydroepiandrosterone, estradiol, and estriol in amniotic fluid throughout gestation. 16 21

Urinary estrogen profiles were made on 6 women, aged 26-30 years. Mean values of excreted estrone (E1) were the highest values in the 1st half of the cycle: 10.15 in the follicular phase and 10.23 mcg/24 hours in midcycle. In the 2nd half of the cycle the level of E1 decreased: 8.78 in the early luteal phase and 8.36 in the late luteal phase. Estradiol (E2) showed its highest mean level in the midcycle, 4.53 mcg, 2.80 in the follicular phase, 3.95 mcg in the early luteal phase, and 3.38 mcg in the late luteal phase. Estriol (E3) showed its lowest levels in the follicular phase at 13.78 mcg and in the late luteal phase at 14.12 mcg/24 hours. The highest E3 levels were 17.59 mcg in midcycle and 17.33 mcg/24 hours in the early luteal phase. The mean quotient ratio of E3/E1+E2 (R) showed high estriol proportions of 1.1, 1.2, 1.4, and 1.2 in all consecutive cycle phases. These are noted to be higher than those of English women (.70 and 1.21 in the 1st and 2nd phases). The racial and geographical factors involved in this are examined.
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PMID:[Urinary estrogen profile in consecutive phases of menstrual cycle in young healthy women]. 86 76

The changes in unconjugated estradiol-17beta and estriol, progesterone and chorionic somatomammotropin (HCS) in peripheral plasma have been studied in 18 women at 30-minute intervals following intra-uterine prostaglandin E2 administration for therapeutic termination of second trimester pregnancy. The hormonal changes were related to the time of fetal death detected by the disappearance of fetal heart pulsations. Prostaglandin E2 was given by the intra-amniotic route with urea (5 patients) or with intravenous oxytocin (5 patients), or by the extra-amniotic route with intravenous oxytocin (8 patients). Fetal death occurred rapidly with intra-amniotic PGE2, but usually at a late stage with extra-amniotic PGE2. Three fetuses in the extra-amniotic group died at or just before abortion. A variety of fetal heart changes were noted and the time of fetal death did not appear to influence the time of abortion within each treatment subgroup. Estradiol and estriol showed a sligh but persistent fall over 24 hours prior to induction of abortion. A more rapid fall usually occurred after induction, with a consistent fall around the time of fetal death. Progesterone and HCS usually fell much less before and immediately after fetal death. A marked rise in estradiol sometimes occurred before fetal death, particularly in the intraamniotic PGE2 and urea subgroup. Estriol levels declined more rapidly before than after fetal death, whereas fetal death had less consistent effects on the other hormones. All hormones had usually fallen considerably at the time of abortion, and in some individuals marked fluctuations in hormone levels were seen.
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PMID:Hormone changes in relation to the time of fetal death after prostaglandin-induced abortion. 88 4

The first successful analysis of estrogens in serum and urine was performed by mass fragmentography using a GC-MS combined system. The equipment used was Shimadzu LKB 9000 GC-MS (MID-PM). The TMSi derivative of the compounds were analyzed using the GC-MS system equipped with a 3 ft x 3mm column packed with 1.5% OV-1 and the temperature was programed from 200 degrees to 260 degrees C at 10 degrees C/min increments. The mass spectrum showed molecular ions at m/e 342, 416 and 504 which correspond to the TMSi derivatives of Estrone (E-1), Estradiol (E-2) and Estriol (E-3) respectively. Molecular ion peak of each compound was applied to establish the precise quantitative evaluation of E-1, E-2 and E-3. 1) The minimum detectable limits of the compounds injected into the column were ca. 2 pg for E-1, E-2 and 5 pg for E-3 respectively. 2) The sensitivity was of the order of ng or pg which enables quantitation with 2 ml of human serum and urine samples obtained from normally ovulating women. 3) This method was very convenient for extracting the compounds from biological fluids, and the procedure can be carried out easily in a short time. 4) Mass fragmentography makes possible the simultaneous measurements of E-1, E-2 and E-3 in samples obtained from pregnant women.
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PMID:[Analysis of estrone, estradiol and estriol in serum and urine by mass fragmentography using GC-MS (author's transl)]. 91 99

The effects of estrogens on electrolyte balances were studied in dogs. In doses of 1 mg or 250 mug/day, 17 beta-estradiol produced moderate sodium retention, whereas 100 mug/day produced only slight sodium retention. Estriol produced about the same degree of sodium retention as did estradiol. The administration of estradiol during the injection of large doses of DOCA produced the same degree of sodium retention as estradiol administered alone. Also, the injection of DOCA to estrogen-treated dogs resulted in a transitory sodium retention, followed by a sodium escape and a return to the previous balance level. Estradiol given to dogs with an arteriovenous shunt that had failed previously to show sodium escape during treatment with DOCA produced the same degree of sodium retention as that observed during estradiol administration to normal dogs. Five adrenalectomized dogs maintained on cortisone and DOCA had normal sodium balances during the control period but showed a retention of sodium during the administration of estradiol; administration. Four adrenalectomized dogs maintained only on cortisone were in negative sodium balance during the control period, but during estradiol treatment they showed a retention of sodium. These studies provide evidence that estrogens promote sodium retention in dogs by mechanisms other than by decreasing the glomerular filtration rate, increasing the secretion rates of adrenal steroids, or affecting the sodium escape mechanism. It is suggested that estrogens might act directly on the renal tubules at receptors other than those for the adrenal mineralocorticoids to produce sodium retention.
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PMID:The effect of estrogens on renal sodium excretion in the dog. 100 38

Estradiol produces both hypertrophic and hyperplastic changes in the uterus, and these changes are associated with alterations in the structure of collagen in the lamina propria. Estriol induces only hypertrophic responses in the immature rat uterus; its effects on collagen structure were characterized in this study. Light micrographs of Masson's trichrome-stained sections revealed that the intensity of the collagen stain in the lamina propria of the rat uterus was profoundly reduced, relative to that in controls, 4 h after estriol (40 micrograms/kg) administration. These changes were not evident 24 h after estriol administration. In control uteri, transmission electron micrographs revealed that the collagen fibers surrounding stromal cells formed dense collections of bundles that were seen throughout the extracellular matrix, whereas in tissues exposed to estriol 4 h earlier, large regions of the extracellular spaces were devoid of collagen bundles. The 4-h changes in collagen were eliminated when animals were pretreated with actinomycin D (8 mg/kg) or cycloheximide (4 mg/kg). Dense collections of collagen bundles were present in tissues 24 h after estriol treatment, and their appearance was not altered by actinomycin D or cycloheximide treatment. Alterations in collagen 4 h after hormone administration appeared to be estrogen-specific since dexamethasone (600 micrograms/kg) and dihydrotestosterone (400 micrograms/kg) had no effect. These data provide evidence that the changes in collagen structure in the uterus are associated with events that function during the hypertrophic growth responses induced by estrogens.
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PMID:Effect of estriol on the structure and organization of collagen in the lamina propria of the immature rat uterus. 163 52

The effects of estriol on serum prolactin (PRL) and LH levels, on the pituitary response to TRH and LHRH and on the synthesis and release of PRL from the anterior pituitary gland were investigated in female rats. The increase of serum PRL levels after estradiol administration was found to be associated with an increase of glutamic acid decarboxylase (GAD) and GABA-transaminase (GABA-T) in the hypothalamus. Thus, a study was carried out on the effects of estradiol and estriol on PRL secretion and on GAD, GABA-T and gamma-amino butyric acid (GABA) in the hypothalamus and the anterior pituitary. Under basal and TRH-stimulated conditions, estriol increased serum PRL levels, decreased basal serum LH levels, and increased the response to LHRH, in terms of LH release. Estradiol and estriol increased the synthesis and release of 3H-PRL from hemipituitary glands in incubations of pretreated animals. Both estrogens induced hyperprolactinemia, concomitantly with an increase of hypothalamic GAD and GABA-T activity. Estriol increased hypothalamic GABA concentration, but did not modify GABA concentration in the pituitary glands. Our results show that estriol, at relatively high doses, seems to be active in increasing PRL synthesis and release and in decreasing serum LH levels; it can also modify pituitary response to TRH and LHRH stimulation.
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PMID:Estriol affects prolactin and LH secretion in rats. 250 80

The reactions of four anti-sex hormone (Estrone, Estradiol, Estriol and Testosterone) antisera were immunohistochemically examined in 109 cancerous and 80 normal and benign thyroid tissues. Four kinds of sex hormones were detected in the tumour cells of 61 cases (56%) of thyroid cancer and in the follicular epithelial cells of 4 cases (5%) of normal and benign thyroid tissues. Among the thyroid cancers, 54 female (61%) and 7 cases in males (33%) were positive for sex hormones. Furthermore, estrogen binding activity was screened histochemically in 36 thyroid tissues of various types, and detected not only in thyroid cancer (6/15 cases), but in normal and benign thyroid tissues (4/21 cases) as well. It was concluded that endogenous estradiol was located in thyroid cancers more frequently in females than in males and that there was estrogen binding activity in the cells of not only thyroid cancers, but also normal and benign thyroid tissues. This is the first report of the demonstration of endogenous sex hormones in thyroid cancer.
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PMID:Endogenous sex hormone and estrogen binding activity in thyroid cancer. 252 Apr 45

Using the "Bi-Digital O-Ring Test Imaging Technique", the author has been able to accurately localize meridians and acupuncture points that correspond to specific internal organs and has found that most general patterns of meridians and the number of acupuncture points on each of the meridians of specific internal organs of the 12 main internal organs described in the literature of ancient Chinese medicine, are more or less correct, with the exception of some variations and inaccuracies. Each meridian of specific internal organs was found to be connected to the organ representation area in the cerebral cortex of specific internal organs. The acupuncture point has an area and occupies 3-dimensional space. It has a circular or slightly oval boundary with diameter in the range of 3 mm to 2.7 cm, although 6-12 mm are the most common diameters in human adults, with the exception of the area outside the corners of the nailbeds of the fingers and toes. Using the "Bi-Digital O-Ring Test Molecular Identification Method", the author also found that within the boundary of most acupuncture points and meridian lines (including Heart, Stomach, and Triple Burner) were high concentrations of neurotransmitters and hormones, including Acetylcholine, Methionine-Enkephalin, Beta-Endorphin, ACTH, Secretin, Cholecystokinin, Norepinephrine, Serotonin, and GABA. On all these meridian lines, in addition to the above neurotransmitters and hormones, Dopamine, Dynorphin 1-13, Prostaglandin E1 (PGE1) and VIP were found, but the latter do not usually exist within the boundary of the acupuncture point with the exception of the center midline of the acupuncture point where the meridian line is situated. Serotonin, Norepinephrine, and Cholecystokinin appeared in either one of the above 2 patterns, depending on the individual. Usually, no significant amounts of these neurotransmitters and hormones were found at the surrounding area outside of meridian and acupuncture points. However, the essential amino acid L-Tryptophan (which is a precursor of Serotonin), was usually found outside of the boundary of the acupuncture point and the meridian but not within the boundary of the acupuncture point and the meridian. Wherever Serotonin appeared, L-Tryptophan disappeared significantly and when the Serotonin disappeared, L-Tryptophan reappeared. In addition to the above common neurotransmitters and hormones, the Heart meridian had additional Atrial Natriuretic Peptide in both the meridian and its acupuncture points. Similarly, the Stomach meridian had additional Gastrin in both the meridian and its acupuncture points. Likewise,the Triple Burner meridian had additional Testosterone (in the male) and Estrogen (especially Estriol and Estradiol in the female.
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PMID:Connections found between each meridian (heart, stomach, triple burner, etc.) & organ representation area of corresponding internal organs in each side of the cerebral cortex; release of common neurotransmitters and hormones unique to each meridian and corresponding acupuncture point & internal organ after acupuncture, electrical stimulation, mechanical stimulation (including shiatsu), soft laser stimulation or QI Gong. 257 47

Mammary carcinomas have been induced by 3.5 Gy whole-body gamma radiation administered at age 40 to 50 days to virgin female Sprague-Dawley rats. In 142 irradiated controls carcinoma incidence averaged 7.8% in survivors observed less than 300 days and 38.3% of those surviving longer (P less than 0.001 by t test). Mammary cancer promotion was inhibited by two methods: estriol (E3) 638 micrograms/month (2.2 microns/mo) subcutaneously for natural life span begun 2 weeks after exposure reduced cancer incidence from 76% in controls to 48% after 331 to 449 mean days observation until neoplasia was palpable (P less than 0.02 by chi-square analysis). Uterine weights were similar in control and treated groups, and were 15% to 18% greater than uteri of nonirradiated controls from other simultaneous experiments. Six monthly 638-micrograms doses of 17 alpha ethinyl estriol (EE3) reduced tumors from 88% in controls to 64% (P less than 0.05 by chi-square analysis) and delayed cancer onset (P less than 0.01-0.04 by life table analysis). Ethinyl estradiol (EE2) after 6 months' treatment similarly delayed mammary tumor development reducing incidence to 75% (NS), with a six-fold increase in nonmammary epithelial malignant tumors. Estriol administration begun between 3 days before to 5 days after radiation did not alter mammary cancer incidence in six experiments. Monthly implantation of 2.5 mg tamoxifen (4.44 microns/mo) started 2 weeks after radiation reduced mammary cancer incidence from 83% to 14% after 307 to 314 days' observation (P less than 0.001 by chi-square analysis). Treated rats had atrophic ovaries and uteri consistent with blockade of endogenous estradiol activity. Short-term parenteral E3 or EE3 therapy using 10 to 30 micrograms/kg/day (35-100 microns/kg/day) rapidly differentiated virgin rat mammary glands without impairment of subsequent estrus cycles and offers an alternative to castration or life-long antiestrogen therapy for reduction of risk of radiogenic mammary carcinoma.
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PMID:Inhibition of radiogenic mammary carcinoma in rats by estriol or tamoxifen. 270 80


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