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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of 11 different steroid hormones on in vitro development of fertilizing capacity by hamster sperm were examined. Capicitation of epididymal sperm occurred only in the presence of female genital tract secretions. Fertilizing ability of sperm was poor if estradiol-17beta, cortisol, chlormadinone acetate, medroxyprogesterone acetate, or megestrol acetate were present in the incubation medium at 10-5M, whereas similar concentrations of estradiol-17alpha, progesterone, norethisterone acetate, ethynodiol diacetate, or norgestrel had little effect. Testosterone was a weak inhibitor of capacitation. Capacitation activity of the female uterus and oviduct washings was higher at estrus than diestrus. This activity was reduced by treating intact animals with progesterone, cortisol, or testosterone, but increased by estradiol-17beta, or HCG. Estradiol-17alpha had no effect. Activity was low in pregnant or ovariectomized hamsters. Treatment of ovariectomized animals with estradiol-17beta increased capacitation activity, but estradiol-17alpha, HCG, or progesterone treatment was ineffective.
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PMID:Steroid hormones and the fertilizing capacity of spermatozoa. 412 1

The effects of estradiol-17 beta on androgen uptake, metabolism and binding were studied in rat epididymis in vivo in comparison with cyproterone acetate. Steroids (250 ug/100 g body weight) were injected 5 min prior to 3H-testosterone in castrate rats. Estradiol-17 beta inhibited 3H-testosterone uptake into epididymal cytosol by 58% as compared to 38% by cyproterone acetate. 3H-Testosterone uptake into epididymal nuclei was inhibited 95% by estradiol-17 beta and 83% by cyproterone acetate. Total bound radioactivity in cytosol fractions was reduced to a greater extent by estradiol-17 beta than cyproterone acetate when either 3H-testosterone or 3H-dihydrotestosterone was injected. Binding of 3H-dihydrotestosterone to nuclear receptors was completely abolished by estradiol-17 beta; whereas approximately 20% binding remained in the nuclear extract after cyproterone acetate treatment. Metabolism of 3H-testosterone in vivo was also altered by estradiol-17 beta, resulting in diminished conversion to 3H-dihydrotestosterone. Cyproterone acetate, on the other hand, did not affect 3H-testosterone metabolism. Estradiol-17 beta and cyproterone acetate inhibited in vitro binding of 3H-dihydrotestosterone to the intracellular cytoplasmic receptor, but not the intraluminal androgen binding protein (ABP). These data suggest that estradiol-17 beta may have a more potent antiandrogenic effect on the epididymis than cyproterone acetate due to inhibition of 5 alpha reduction of testosterone as well as binding to the androgen receptor.
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PMID:Estradiol-17 beta inhibition of androgen uptake, metabolism and binding in epididymis of adult male rats in vivo: a comparison with cyproterone acetate. 645 38

The effects of 17 beta-estradiol and testosterone administration on cholesterol esterase, lipoprotein lipase activities and adrenalin-induced lipolysis were examined in rat adipose tissues with the change in serum lipid level. The administration of 17 beta-estradiol (500 micrograms/kg, 2 or 4 weeks) to male rats significantly reduced the body weight, and markedly increased serum cholesterol, triacylglycerols and phospholipids. Cholesterol esterase activity was significantly enhanced in the epididymal adipose tissue from estradiol treated rats and the effect was greater with duration of the treatment. In contrast, lipoprotein lipase activity was markedly reduced. Testosterone reduced cholesterol esterase activity in the parametrial adipose tissue through the treatment with 500 micrograms/kg for 6 weeks, but it did neither influence serum lipids nor lipoprotein lipase activity. Basal lipolysis and adrenalin-induced lipolysis were also significantly enhanced in the epididymal adipose tissue from the male rat treated either with 7 mg/kg estradiol 12 h ahead or with 500 micrograms/kg estradiol for 2 weeks. These results indicate that estradiol exerts strong effects on metabolism of the adipose and these effects seems to be mediated through cyclic-AMP. An alteration of adrenergic functions by gonadal steroids might be intervened.
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PMID:Enhancement in cholesterol-esterase activity and lipolysis due to 17 beta-estradiol treatment in rat adipose tissue. 650 Apr 87

The androgen-binding protein (ABP) and the cytosol androgen receptor (Rc) were measured in the epididymis of sheep aged 50, 120 and 200 days. Specific binding protein was not detected at 50 days (infantile); near puberty (120 days), ABP was more concentrated in caput and cauda epididymal cytosols (117 and 183 fmol/mg protein respectively) than in corpus (53 fmol/mg) although Rc levels were low (3-5 fmol/mg). In postpubertal rams (200 days), ABP and Rc concentrations were higher in caput and cauda than in corpus epididymis. Testosterone concentrations at 50 days were not statistically different along the epididymis and varied from 0.3 to 0.8 pmol/mg protein. In 120-day-old animals, testosterone was more concentrated in caput and corpus (0.45 and 0.41 pmol/mg) than in cauda (0.17 pmol/mg); at 200 days, the testosterone contents were low (0.10-0.17 pmol/mg) in all parts of the epididymis. A ten-fold increase in plasma testosterone concentrations was observed between 50 and 200 days (1.31 to 11.71 nmol/l). Histological studies of the epididymis in the three groups of animals showed that the cell differentiation started in the cauda where the principal epithelial cells were higher (47-56 micron) than in the caput (31-38 micron) at 50 days. The principal cells of the caput were two- to threefold higher in postpubertal rams than in infantile lambs, a finding which is correlated with the levels of ABP and Rc. This may suggest an important physiological role of this region in the induction of sperm maturation.
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PMID:Androgen-binding proteins in sheep epididymis: age-related effects on androgen-binding protein, cytosolic androgen receptor and testosterone concentrations. Correlations with histological studies. 654 25

The levels of testosterone (T) and 17-beta-estradiol (E2) in seminal plasma were determined by the direct RIA method with tritium-labelled testosterone and 17-beta-estradiol. Testosterone was determined in 47 ejaculates and E2 in 132 ejaculates of seven bulls whose age ranged from 10 to 26 months, and in 60 ejaculates of two breeding boars old 20 months. The seminal plasma of bulls was found to contain 2.09 +/- 1.67 nmol/l testosterone and 2.75 +/- 1.94 nmol/l E2. Without respect to the age of the sires, the marginal values of the studied steroids showed a comparatively high fluctuation so that the average values are not very different between individual animals. No relation was found between the level of steroids and the concentration of fructose; this applies to the fertile bulls as well as to the bull suffering from epididymitis with the formation of epididymal cysts. Breeding boars had 0.338 nmol/ E2 (+/- 0.3) and 6.40 +/- 4.01 nmol/l testosterone in their seminal plasma. When the obtained values are recalculated to an average ejaculate volume, 5 ml of the seminal plasma of bulls will contain about 0.013 nmol E2 and 0.010 nmol T and 300 ml of the seminal plasma of boars will contain about 0.101 nmol E2 and 1.920 nmol T.
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PMID:[Levels of testosterone and 17-beta estradiol in the seminal plasma of bulls and boars]. 681 48

Previous investigations have established the production of specific epididymal proteins (SEP) in the rat which become attached to the sperm surface as these cells pass along the duct. The present study is concerned with the regulation of SEP synthesis by androgens. For this purpose, we determined the concentrations of SEP and protein DE, one of its main components (40%), during sexual maturation, after castration with and without androgen administration, and after ligation of the efferent ductuli in rats. SEP were first detectable at 25 days of age and attained adult values at 60-90 days of age. Protein DE behaved similarly. Castration of the adult rat led to a decrease in SEP and DE concentrations. The fall was more rapid and marked in the caput than in the caudal segments. SEP synthesis seemed to stop promptly after castration; the different rates of decrease of SEP in caput and cauda may reflect different rates of exit of spermatozoa from those segments. SEP and DE concentrations in castrated rats were increased by the administration of testosterone (100 micrograms/day). The SEP concentration was increased after 4 days and restored to control values after 11 days of treatment. Testosterone and 5 alpha-dihydrotestosterone were equipotent in inducing SEP and DE synthesis, while 5 alpha-androstandiols were less potent. The effects of androgens were significantly reduced by the simultaneous administration of cyproterone acetate. We propose that SEP is a suitable marker for following the action of androgens in the epididymis.
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PMID:Androgen-controlled synthesis of specific proteins in the rat epididymis. 683 62

Testosterone (T) and dihydrotestosterone (DHT) were measured in the seminal plasma of men with varicoceles, azoospermic vasectomized men and men with normal seminal parameters. Testosterone levels were not different significantly in these groups of men. DHT concentrations and the DHT/T ratio were significantly lower than normal in men with varicoceles and sperm densities below 30 million/ml and the vasectomized men, but not different from normal in the men with varicoceles whose sperm densities were greater than 30 million/ml. In men whose sperm density and/or motility improved after varicocelectomy, there was an increase in seminal plasma DHT levels and the DHT/T ratio. When seminal parameters were not improved by varicocelectomy, there was no change in DHT levels or in the DHT/T ratio. It is concluded that men with varicoceles and sperm densities below 30 million/ml have a deficiency in the epididymal 5 alpha-reduction of testosterone.
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PMID:Seminal plasma testosterone and dihydrotestosterone levels in men with varicoceles. 686 70

Testosterone and androstenedione were measured in testicular and epididymal tissue of 37 previously healthy infants between 1 and 24 months of age who died suddenly. In half of the patients elevated plasma levels of cortisol and androstenedione suggested preterminal stress. Plasma testosterone levels, however, did not differ from those in healthy infants. Testicular testosterone concentrations were maximal in boys from 1-3 months of age (median, 36.6 ng/g; range, 7-380 ng/g) with peak values similar to those found in pubertal or even adult testes. Thereafter testicular testosterone concentrations decreased and after the age of 6 months all values were below 12.5 ng/g, which corresponds to the low normal range of older prepubertal boys. Plasma testosterone and testicular testosterone correlated significantly (P less than 0.001). On average the testicular concentrations were 36.4 times higher than the corresponding plasma concentrations. Testicular androstenedione was low but correlated significantly with testicular testosterone (P less than 0.001). Epididymal testosterone concentrations were surprisingly high (1-3 months: median, 10.3 ng/g; range, 4-42.7 ng/g) and averaged 30% of the testicular testosterone concentration. Thus, epididymal testosterone concentrations were significantly higher than the circulating plasma testosterone levels, indicating the capacity of the infant epididymis to accumulate androgens. These findings suggest that high local testosterone concentrations during early infancy are important not only for the testis itself but particularly for the developing epididymis.
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PMID:Testosterone and androstenedione concentrations in human testis and epididymis during the first two years of life. 686 78

Male rats rendered diabetic by IV streptozotocin (65 mg/kg body weight) were treated with exogenous insulin or testosterone. Charcoal-coated dextran and polyacrylemide gel electrophoresis techniques were employed in studying the characteristics of androgen (R1881) binding to prostate cytosol protein. In comparison with normal (N) rats, the replacement therapy of diabetic (D) animals with insulin (D + I) or testosterone (D + T) was able to restore epididymal weight (N = 0.40 +/- 0.04 g; D = 0.18 +/0 0.02 g; D + I = 0.42 +/- 0.05 g; D + T = 0.40 +/0 0.06 g) and total prostate weight (N = 0.24 +/- 0.02 g; D = 0.15 +/- 0.02 g; D + I = 0.24 +/- 0.05 g; D + T = 0.35 +/- 0.06 h). Testicular endogenous content of testosterone was restored after insulin treatment (N = 154 +/- 13 ng/testis; D = 41 +/- 5 ng/testis; D + I = 142 +/- 9 ng/testis), and significant improvements of serum testosterone levels were also achieved (N = 540 +/- 64 ng/100 ml; D = 238 +/- 37 ng/100 ml; D + I = 358 +/- 18 ng/100 ml). Prostate cytosol of streptozotocin-diabetic rats had strongly lowered capacity for 3H-R1881 binding compared with controls (94 and 12 fmol/mg protein, respectively). Testosterone treatment produced a 3.3-fold improvement of this lowered value, whereas the increment seen with insulin was less (1.5-fold). It is emphasized that some of the improvements caused by insulin replacement therapy in diabetic animals are due to the partial restoration of testosterone secretion. Thus, the combined actions of insulin and testosterone (instead of insulin alone) seem to be of major importance in the maintenance and regulation of accessory sex glands function.
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PMID:Androgen receptors in the diabetic rat. 696 99

Studies were undertaken to evaluate the direct insulin-like action of S enteritidis endotoxin on glucose oxidation in the rat epididymal fat pad and to assess antagonism by steroidal and nonsteroidal anti-inflammatory agents. In vitro administration of endotoxin at concentrations of 500, 100, 50, and 10 micrograms/ml significantly increased adipose tissue glucose oxidation by 115, 92, 55, and 32%, respectively. Exposure of the fat pads to endotoxin (100 microgram/ml) for timed incubations of 120 to 5 min, all produced significant increments in glucose oxidation. The insulin-like action of endotoxin was significantly less in Ca2+ free-KRB plus EGTA. Cotreatment of the fat pads with endotoxin and the steroidal anti-inflammatory agents, dexamethasone and methylprednisolone, as well as the nonsteroidal anti-inflammatory agent, indomethacin, significantly antagonized endotoxin-stimulated glucose oxidation. Dexamethasone antagonism was not significant if it was added after endotoxin treatment. Testosterone, a steroid with no anti-inflammatory activity, did not antagonize endotoxin's insulin-like action. The data provide further evidence of the direct insulin-like action of endotoxin and suggest that the protective effect of dexamethasone, methylprednisolone, and indomethacin may be due, in part, to a direct antagonism of endotoxin at the tissue level.
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PMID:Insulin-like action of endotoxin: antagonism by steroidal and nonsteroidal anti-inflammatory agents. 702 80


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