Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estrogen binding activity was investigated in the epididymis of the turtle, Chrysemys picta using DNA-cellulose affinity chromatography. A component binding estradiol-17 beta specifically with high affinity (Kd:8.0 X 10(-10) M) and limited capacity (20 fmol/mg protein) was demonstrated in the epididymal cytosol. In addition, binding of estradiol-17 beta was sensitive to excess (100-fold) diethylstilbestrol or natural estrogens (estradiol-17 beta, estrone, and estriol) but not to progesterone or androgens (testosterone and 5 alpha-dihydrotestosterone). The specific estrogen binding macromolecules eluted from DNA-cellulose columns sedimented at 4-5 S in linear 5-20% sucrose gradients. These characteristics suggest the presence of an estrogen receptor in this androgen target organ.
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PMID:Estradiol binding activity in epididymal cytosol of the turtle, Chrysemys picta. 688 62

The concentrations of testosterone, four of its precursors (pregnenolone, progesterone, 17 alpha-hydroxyprogesterone, and androstenedione), and three of its metabolites (5 alpha-dihydrotesterone, 5 alpha-androstane-3 alpha, 17 beta-diol, and androsterone) were measured in the epididymis and proximal ductus deferens of elderly men with prostatic carcinoma. In addition, they were measured in testis tissue and spermatic and p eripheral blood sera.l The main androgen in the epididymis was testosterone [37.3 +/- 22.0 (SD) ng/g wet tissue]; 5 alpha-dihydrotestosterone was also present in a relatively high concentration [9.7 +/- 6.5 (SD) ng/g wet tissue]. There were no steroid concentration gradients along the epididymis. The actual and relative concentrations of the steroids measured strongly suggest that they are transferred from testes to epididymides in the testicular lymph or rete testis fluid. Estrogen administration led to significant decreases in epididymal androstenedione, testosterone, and 5 alpha-dihydrotestosterone concentrations. Thus, one facet of the deleterious effects of estrogen on male reproductive functions may be interference with normal epididymal function, essential for undisturbed sperm maturation.
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PMID:Testosterone and some of its precursors and metabolites in the human epididymis. 741 May 27

Male rat adipose tissues contain cytoplasmic estrogen binding sites comparable to those found in females. This bindng is of high affinity (Kd = 1.7 x 10(-10) M) and is estrogen specific. Binding of 17 beta-estradiol was inhibited by radioinert estrogens (17 beta-estradiol and R 2858) but not by other steroids (progesterone, 5 alpha-dihydrotestosterone, and corticosterone). Estrogen binding sites were found in all fat pads studied, but levels were highest in the epididymal pads. Treatment of female rats with 17 beta-estradiol benzoate (E2B) induced cytoplasmic progestin receptors in adipose tissues, but in three separate experiments, E2B treatment (20 microgram/day for 3 days) failed to induce measurable progestin ([3H]R 5020) binding sites in males. E2B treatment reduced lipoprotein lipase (LPL) activity by approximately 75% in epididymal (male) and parametrial (female) fat pads. Concurrent progesterone treatment increased parametrial LPL activity in E2B-treated females, but progesterone had no effect on epididymal fat pad LPL activity in males. These findings are consistent with the hypothesis that in male rats aromatized (estrogenic) metabolites of testosterone may reduce body fat content and alter lipid metabolism by direct actions on adipose tissues.
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PMID:Cytoplasmic estrogen, but not progestin, binding sites in male rat adipose tissues. 742 16

Estrogen binding sites (ER) were studied, using 17 beta-[3H]estradiol as the ligand, in epididymal or parametrial and subcutaneous adipose tissues of male and female hamsters. Compared with other mammalian fat deposits, intact male and female hamsters possess abundant estrogen binding sites with moderate affinity for estradiol and which occur as a single class of receptor in males but as two populations in females. The levels of estrogen receptors depend on both sex and tissue localization. In males, receptor densities are higher in both localizations when compared to those of females and ER are more abundant in superficial adipose deposits than in the deep fat tissue. In females, there are two estrogen binding populations; the one with the highest affinity is similar to the classical estrogen receptor and both populations are more abundant in deep fat than in subcutaneous deposits, in contrast to male hamsters. These characteristics depend on androgen status: in male adipose tissues, testosterone (TP) up-regulates the ER levels. Conversely, in female fat deposits, TP down-regulates the highest affinity estrogen receptors and the lowest affinity population disappears. Binding affinities are never affected by testosterone. These results suggest that, in hamster adipose tissue, estrogen receptors exhibit site- and sex-related differences, as previously described for androgen receptors. Furthermore, estrogen receptor expression is modulated by the androgen status, depending on gender, which could be related to some physiological situations observed in the hamster.
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PMID:Estrogen binding sites in hamster white adipose tissue: sex- and site-related variations; modulation by testosterone. 858 99

Recent studies reported from our laboratory have established that the sustained delivery of danazol in combination with androgens resulted in the remarkable reduction of epididymal mass. In addition, previous studies have recommended that ultrastructural of epididymal tubules have to be elucidated. The specific objective of this investigation was to evaluate the cytological characteristics of epididymal tissues exposed to sustained delivery of dihydrotestosterone (DHT), dehydroepiandrsterone (DHEA) and a combination of Estrogen (E), DHEA plus DHT by means of tricalcium phosphate lysine (TCPL) delivery system. Adult male rats (BW 300-350 gm) were randomly divided into four equal groups: Group I animals were implanted i.p. with TCPL loaded with DHEA (100 mg). Animals in group II were implanted with TCPL capsules loaded with DHEA (100 mg) + DHT (500 mg). Group III animals were implanted with TCPL capsules loaded with E (200 mg) + DHEA (100 mg) + DHT (500 mg). Group IV animals served as the intact unimplanted controls. Surgical aseptic techniques were performed according to standard laboratory procedures. The animals were maintained at the University of Mississippi Medical Center Animal Facilities following the rules and regulations established by NIH on the Care and Use of Laboratory animals. At the end of 6 weeks post implantation, all animals were sacrificed and the epididymal tissues were collected, weighed, and embedded for histopathological evaluations. Statistical analysis was conducted by using standard computer programs (STATVIEW, ANOVA at 95% CI). The data obtained in this investigation demonstrated the following: (1) remarkable reduction in sperm counts and motility obtained from epididymal tubules in all experimental (hormonally treated) groups, (2) the lumen of the epididymal tubules were devoid of sperm in animals treated with DHT in comparison to the control, (3) a decrease in the diameter of tubules with occasional hypertrophic epithelium in all experimental animals, (4) disorganization of nuclear material was observed in animals treated with DHEA and DHEA + E + DHT in comparison to the control group. The overall observation of this study suggests that sustained delivery of DHEA, DHEA + DHT, and DHEA + DHT + E can be used to regulate the structural and functional architecture of the site of extramaturation of spermatozoa.
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PMID:TCPL delivery system: the role of DHT, DHEA, and E on the epididymal tubules of adult male rats. 960 9

Vacuolar type H(+)-ATPase is involved in lumenal acidification of the epididymis. This protein is highly expressed in narrow and clear cells where it is located in the apical pole, and it contributes to proton secretion into the lumen. We have previously shown that in rats, epididymal cells rich in H(+)ATPase appear during postnatal development and reach maximal numbers at 3-4 wk of age. The factors that regulate the appearance of these cells have not been investigated, but androgens, estrogens, or both may be involved. This study examined whether neonatal administration of estrogens (diethylstilbestrol [DES] or ethinyl estradiol) or an antiandrogen (flutamide), or the suppression of androgen production via administration of a GnRH antagonist (GnRHa), was able to alter the appearance of cells rich in H(+)-ATPase in the rat epididymis when assessed at age 25 days. Surprisingly, all of these treatments were able to significantly reduce the number of H(+)-ATPase positive cells; this was determined by immunofluorescence and confirmed by Western blotting. In contrast, neonatal coadministration of DES and testosterone maintained the expression of H(+)-ATPase in the epididymis at Day 25 despite the high level of concomitant estrogen exposure. These findings indicate that androgens, acting via the androgen receptor, are essential for the normal development of epididymal cells rich in H(+)-ATPase, and that treatments that interfere directly or indirectly with androgen production (GnRHa, DES) or action (flutamide, DES) will result in reduced expression of H(+)-ATPase. Our findings do not exclude the possibility that estrogens can directly suppress the postnatal development of cells in the epididymis that are rich in H(+)-ATPase, but if this is the case, this suppression can be prevented by testosterone administration.
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PMID:Modulation of the onset of postnatal development of H(+)-ATPase-rich cells by steroid hormones in rat epididymis. 1229 25

Before prescribing a "morning after" contraceptive, the practitioner should determine at what point in the cycle the unprotected intercourse took place. The anxiety of the woman should be taken into account in deciding whether to prescribe such a method. In the absence of contraindications, estrogens at high doses should be given if the coitus occurred with 72 hours of the consultation. Distilbene can be given at 50 mg/day for 5 days, or ethinyl estradiol at 5 mg/day for 5 days, or Premarin i.v. at 50 mg/day for 2 days or 25 mg/day for 3 days. The Pearl index for these formulations ranges from 0-2.4. The exceptional nature of the prescription should be explained to the woman in all cases. The practitioner should also be aware of the possibility of prescribing d-Norgestrel at a dose of .6 mg-1 mg taken within 3 hours of intercourse, which is better tolerated than the estrogens and provides a Pearl index of 0-6. Patients given estrogens should be advised that side effects are possible. An antiemetic can be prescribed to lessen the most common side effects of nausea and vomiting. Patients should be advised to take the estrogens during meals. Vaginal adenocarcinoma and epididymal cysts will not occur in children born to mothers who took Distilbene in an effort to avoid pregnancy. The genital teratogenic risk appears to be null before the 6th week of pregnancy. The IUD can be an excellent morning after method if it is inserted within 5 days and all contraindications are respected. The patient should be advised that some changes in the timing and amount of menstrual bleeding may occur. Possible signs of ectopic pregnancy should not be ignored with any postcoital method. The mechanisms of action of the methods are enzymatic modifications of the mucus which opposite nidation in the case of the IUD, and antinidatory modifications of the mucus, anti-corpus luteum activity, or changes in the speed of tubal migration of the egg in the case of the hormonal methods.
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PMID:[In case of a request for "the morning after" pill. Do's and don'ts]. 1231 Apr 6

The present paper is an evaluation of the studies of two articles published in this issue of the journal which adopted a new regimen of low dose gossypol(12 mg.kg-1.d-1) combined with steroid hormones (methyltestosterone 20 mg.kg-1.d-1 and ethinyl estradiol 100 micrograms.kg-1.d-1) for 6 weeks as initial dose, and a similar low dose gossypol alone for 12 weeks as maintenance dose. Results showed that the dosage regimen could damage the epididymal sperms and onset of antifertility within 6 weeks in male rats, and prevent the incidence of the side effect of irreversible azoospermia. There was no adverse effect in viscera tissues, and the infertility could be reversible in about 6 weeks following withdrawal of gossypol. Male volunteers taking low dose gossypol (15 mg/d) could induce antifertility within 12 weeks, then followed by a maintenance dose of gossypol(10 mg/d) for 44 weeks. All of them remained infertile, and without developing hypokalemia and irreversible azoospermia. The fertility and the inducing abnormal histone-to-protamine replacement reaction as well as alteration of nuclear basic proteins could be recovered 10 weeks after withdrawal of drug treatment. These results provide a new approach for using the new regimen in clinical trial and a new prospect of gossypol as a potential male contraceptive.
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PMID:[A beam of dawn light of study on gossypol as a safe, effective, and reversible male antifertility contraceptive--evaluation of the studies by using low dose gossypol combined with steroid hormone for male contraception]. 1290 61

Testosterone and estrogen are no longer considered male only and female only hormones. Both hormones are important in both sexes. It was known as early as the 1930's that developmental exposure to a high dose of estrogen causes malformation of the male reproductive tract, but the early formative years of reproductive biology as a discipline did not recognize the importance of estrogen in regulating the normal function of the adult male reproductive tract. In the adult testis, estrogen is synthesized by Leydig cells and the germ cells, producing a relatively high concentration in rete testis fluid. Estrogen receptors are present in the testis, efferent ductules and epididymis of most species. However, estrogen receptor-alpha is reported absent in the testis of a few species, including man. Estrogen receptors are abundant in the efferent ductule epithelium, where their primary function is to regulate the expression of proteins involved in fluid reabsorption. Disruption of the alpha-receptor, either in the knockout (alphaERKO) or by treatment with a pure antiestrogen, results in dilution of cauda epididymal sperm, disruption of sperm morphology, inhibition of sodium transport and subsequent water reabsorption, increased secretion of Cl-, and eventual decreased fertility. In addition to this primary regulation of luminal fluid and ion transport, estrogen is also responsible for maintaining a differentiated epithelial morphology. Thus, we conclude that estrogen or its alpha-receptor is an absolute necessity for fertility in the male.
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PMID:Estrogen in the adult male reproductive tract: a review. 1290 63

Estrogen plays an essential role in male reproduction. In human and other mammalians, a number of tissues express aromatase and hence synthesize estrogen. ERs and aromatase are present at all developmental stages of the male reproductive organs in many mammalian species. Estrogen is important in different aspects in male reproductive physiology, including its effects on germ cells, Sertoli cells, Leydig cells and epididymal functions.
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PMID:[Role of estrogen in male reproduction]. 1633 67


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