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)

1. Male flounders receiving 100 micrograms estradiol each second day were fully induced to vitellogenin synthesis within 11 days, while fishes given 5 micrograms doses continued to accumulate vitellogenin in the serum at a progressive rate through 17 days. 2. Liver DNA per unit fish remained constant, while RNA per unit fish in flounders given 100 and 5 micrograms doses attained values 80 and 25% respectively, above the values found in control animals. 3. Liver RNA per unit DNA increased at maximal rate within 6 days in fishes receiving 100 micrograms doses. RNA synthesis continued at a progressive rate through 17 days in fishes given 5 micrograms doses of estradiol. 4. Liver protein per unit DNA elevated at a plateau 60% above control within 6 days with 100 micrograms doses. Doses of 5 micrograms had only little effect on liver protein. 5. Estradiol had a lipogenic effect on the liver. Cellular lipid rose 120 and 60% above control after treatment with 100 and 5 micrograms respectively. 6. Liver dry weight per unit DNA increased 60 and 55% above control with 100 and 5 micrograms doses respectively. Cellular hypertrophy in fishes receiving the smaller dose was primarily associated with an increase in lipid concentration, while protein and lipid contributed almost equally to cellular growth in fishes receiving the high dose.
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PMID:Dose response kinetics of serum vitellogenin, liver DNA, RNA, protein and lipid after induction by estradiol-17 beta in male flounders (Platichthys flesus L.). 9 87

Medroxyprogesterone acetate (Provera) was administered orally during 2-4 days to women undergoing endometrial curettage during the follicular phase of the menstrual cycle. Estradiol (E2) receptor levels were estimated from the amounts of 2H-E2 tightly bound in nuclei after incubation of endometrial tissue with an excess of the labeled hormone. An average value (9 subjects) of 1.5 pmole E2/mg DNA +/- 0.7 (mean +1- SD) was found. This value is significantly lower than the average E2 receptor levels in proliferative endometrium of untreated subjects (3.2 +/- 1.3, n = 33) and equals the level observed in the early secretory phase (1.5 +/- 0.5, n = 5). These results indicate that one of the progestin effects on human endometrium is the reduction of E2 receptor levels.
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PMID:Effects of progestins on estradiol receptor levels in human endometrium. 16 81

Estradiol and testosterone binding macromolecules are demonstrated in normal mouse cerebellum. Identity of the estradiol binder as the 'receptor' is provided by its binding to DNA-cellulose, which does not occur for other estradiol binding proteins. The androgen binder is identified as 'receptor' by its specific deficiency (85% reduced) in the androgen-insensitive mutant mouse, testicular feminization (Tfm). The relative amounts of these two components are reversed in cerebellum compared to hypothalamus-preoptic area. Neurological mouse mutants, which lack specified neurons, are examined to test for the cells in which these hormone binding proteins are located. Experiments with Purkinje cell degeneration (pcd), weaver (wv) and staggerer (sg), suggest that the majority of these receptors are present in granule cells.
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PMID:Estradiol and testosterone binding in normal and mutant mouse cerebellum: biochemical and cellular specificity. 19 54

The uterotropic and antiuterotrapic effects of a variety of structural derivatives of the nonsteroidal antiestrogen tamoxifen have been determined in the rat and the mouse. One derivative, monohydroxytamoxifen, was found to be a potent antiestrogen in the rat, with a high affinity for the estrogen receptor. Various techniques of sucrose density gradient analysis were used to demonstrate that estradiol and tamoxifen bind to the rat uterine cytoplasmic estrogen receptor. Estrogens and antiestrogens provoke the translocation of estrogen receptors to the nucleus and deplete the cytoplasmic estrogen receptor pool for short or long periods depending on the dose administered. Estradiol stimulates endometrial hyperplasia with an increase in total uterine DNA content, whereas tamoxifen stimulates endometrial hypertrophy with only a slight increase in uterine DNA content. It is concluded that the molecular shape of the ligand that binds to the estrogen receptor determines antiestrogenic activity.
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PMID:Nonsteroidal antiestrogens: their biological effects and potential mechanisms of action. 20 80

A nuclear subfraction containing bound estrogen receptor in presumed complex with its nuclear acceptor site has been partially purified from hen oviduct. Sucrose density gradient ultracentrifugation was used to separate mechanically sheared chromatin (i.e. lysed nuclei) into several fractions which differed in protein to DNA ratio as well as in vitro template activity. Gradient fractions were then examined for the presence of bound estrogen receptors. Care was taken to use physiological ionic strength buffers when preparing nuclei since the number of estrogen receptors per nucleus decreased from 5600 to 1600 when nuclei prepared in low ionic strength (mu = 0.013 M) were compared with nuclei prepared in physiological ionic strength (mu = 0.2 M). [3H]Estradiol was introduced into nuclear estrogen receptors by exposing minced oviduct to labeled hormone in tissue culture or by exchanging nuclear estrogen receptor complexes formed in vivo with labeled hormone. In all cases, receptor was found in a fast sedimenting nuclear subfraction of low in vitro template activity. Sodium dodecyl sulfate-gel electrophoresis revealed no differences between proteins from receptor-containing and slower sedimenting fractions. Hybrdization experiments using a cDNA probe made from ovalbumin mRNA indicated no enrichment of this gene in DNA from receptor-containing nuclear material. Salt-extracted nuclear estrogen receptor was shown to partially aggregate to fast sedimenting species of heterogeneous size when sedimented in gradients containing low salt concentrations. Bound receptors were distinguished from such receptor aggregates using a novel electrophoresis technique. In addition, receptor aggregates could be disrupted in high salt, while bound receptors were resistant to this treatment. The number of exchangeable nuclear estrogen receptors in immature chicks given secondary estrogen stimulation was compared with birds that had been withdrawn from hormone. The number of receptors per nucleus was shown to be higher in animals given secondary stimulation, and these receptors were associated exclusively with fast sedimenting nuclear material.
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PMID:Isolation of estrogen receptor in complex with a discrete nuclear subfraction from hen oviduct. 42 74

Estradiol-binding proteins with the properties of putative estrogen receptors are present in cytosol extracts of embryonic mouse hypothalamus and other brain regions. These embryonic estrogen receptors are adultlike in their high affinity and limited capacity for estradiol, sensitivity to diethylstilbestrol, ability to adhere to DNA, and behavior during DNA-cellulose affinity chromatography. As early as 4 days before birth, mouse hypothalamus has approximately 40 percent of the adult concentration of hypothalamic estrogen receptors with these properties. These observations raise the possibility that embryonic rodent brain has the biochemical potential to respond to sex hormones and that the critical period of brain sexual differentiation could be initiated prenatally.
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PMID:Embryonic rodent brain contains estrogen receptors. 43 56

Estradiol is likely involved in stimulating developmental changes in the ability of the rat pituitary to secrete prolactin. To investigate the possibility that these changes involve proliferation of prolactin cells, estradiol effects on pituitary growth and prolactin synthesis were examined. Estradiol treatment of immature female rats stimulates increases in pituitary weight, [3H] thymidine incorporation, DNA content and prolactin synthesis. Treatment of rats with the DNA synthesis inhibitor, hydroxyurea, partially blocked the ability of estradiol to stimulate prolactin synthesis suggesting that at least part of the effect of estrogen is due to cell proliferation. These results suggest that estrogen-induced proliferation of prolactin cells is involved in the developmental processes of the pituitary.
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PMID:Estrogen-induced prolactin and DNA synthesis in immature female rat pituitaries. 44 85

Estradiol-binding proteins in the reproductive tract of the turtle, Chrysemys picta, were characterized. Cytosol was prepared from the oviducts of mature female turtles, and estradiol binding was measured using charcoal adsorption and glycerol density gradient centrifugation. A sex steroid-binding protein (SBP) similar to that found in turtle plasma was demonstrated in oviduct cytosol. The characteristics of this SBP-like binding were as follows: Ka = 10(8) M-1; capacity, 10(-12) mol/mg protein; and sedimentation coefficient, 6--7S in low salt gradients. The SBP-like protein binds testosterone and progesterone as well as 17 beta-estradiol but does not bind diethylstilbestrol. No receptor-like binding activity could be demonstrated using these techniques. Explant culture and DNA cellulose affinity chromatography were used to remove the SBP-like material before assay of [3H]estradiol binding. Using these techniques, a high affinity (Ka = 10(9) M-1), low capacity (n = 10(-14) mol/mg cytosol protein) estradiol receptor was demonstrated. The putative turtle receptor exhibits steroid specificity and sedimentation profiles (6S and 8S in low salt, 4S and 5S in high salt) comparable to those of estrogen receptors in mammalian species. These results suggest a certain degree of physiochemical similarity between putative estrogen receptors in mammalian and turtle reproductive tracts.
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PMID:Estrogen-binding proteins in the oviduct of the turtle, Chrysemys picta: evidence for a receptor species. 49 79

Estrogenic hormones first stimulate and then inhibit DNA synthesis in the uterus of the immature rat. Both the stimulatory and the inhibitory effects depend on the sustained presence of estrogen. Thus, estriol, which is equal in effectiveness to estradiol on early (up to 6 hr) responses, has only a partial stimulatory effect on DNA synthesis. Estradiol initially stimulates DNA synthesis, but the sustained presence of this steroid inhibits further synthesis of this macromolecule and cell division. These observations are discussed in terms of their relationship to current models of estrogen action and to estrogen dependency in some types of cancer.
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PMID:Hormone regulation of growth: stimulatory and inhibitory influences of estrogens on DNA synthesis. 56 46

The steroid hormone estradiol, and the glycoprotein hormones follicle-stimulating hormone (FSH) and luteinizing hormone (LH), are known to be essential for the growth and differentiation of follicles in the ovary. The present study was conducted to determine quantitatively the effects of estradiol, FSH and LH on proliferation of different ovarian cell types (granulosa and theca cells). The immature female hypophysectomized rate sequentially primed with estradiol, FSH and LH was used as the experimental model. Proliferation was assessed by examining changes in total DNA, incorporation of 3H-thymidine into DNA and labeling index in specific cell types. Estradiol and FSH each acted on follicles at different stages of development to stimulate proliferative activity of both granulosa and theca cells. Continued administration of either hormone caused a decrease in the proliferative activity of both cell types. These observations have been interpreted to indicate that estradiol and FSH can each alter the length of the specific phases of the cell cycle. A luteinizing dose of LH caused a cessation of proliferation in luteinizing granulosa cells while stimulating a limited proliferation of theca cells. Absence of the appropriate hormonal stimulus caused both granulosa and theca cells to stop proliferating and the follicles to undergo atresia. These results indicate that, depending upon the state of differentiation of granulosa and theca cells, estradiol, FSH and LH can stimulate or inhibit the ability of these cells to proliferate.
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PMID:Hormonal regulation of ovarian cellular proliferation. 56 19


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