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)

The specific activities of three acid phosphatases were followed in the epididymis of growing rats. All activities were constantly rising but revealed two steeper parts probably corresponding to the increase of androgen secretion and the arrival of spermatozoa in the epididymis. Simultaneously an increase in the histochemical staining was obtained in all epididymal segments. Both biochemical and histochemical studies showed that castration reduced the activity of all acid phosphatases and this could be restored with testosterone-estradiol treatment. Estradiol had no effect on the activities in the castrated animal, but in the normal animal it caused an elevation of Enzyme I activity. In the histochemical study estradiol seemed to restore the acid phosphatase activity. Enzyme I reacted slower than the others to both castration and hormone treatment. Increased elimination caused by ligation of the epididymis caused a reduction in the activity of all enzymes within four days. It was greatest in the area of the corpus. This study, however, rendered no further elucidation for the assumption that acid phosphatases participate in the elimination of excessive and defective spermatozoa.
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PMID:Acid phosphatase of the rat epididymis. III. Histochemical and biochemical responses in experimental conditions. 59 63

The nuclear estrogen receptor was characterised in isolated rat adipocytes. The binding reaction with [3H]estradiol was performed with intact isolated rat adipocytes and the radioactivity associated with the nucleus was subsequently determined after cell lysis. The nuclear uptake of [3H]estrogen in rat adipocytes was temperature dependent and steroid specific. The steady-state binding was achieved after 30 min at 37 degrees C and was constant for several hours. Estradiol was found to bind to a homogeneous class of nuclear receptors in epididymal adipocytes with an apparent Kd of 3.1 +/- 0.76 nM and a Bmax of 7.98 +/- 1.11 fmol/10(6) cells corresponding to about 4800 receptors per nucleus. The estradiol binding exhibited regional variations in isolated adipocytes. In lean rats the highest receptor number was found in epididymal adipocytes, whereas there was a significantly lower number of nuclear binding sites in perirenal and subcutaneous adipocytes (P less than 0.05), unlike in older and more obese rats where the nuclear estradiol binding was greatest in adipocytes from the perirenal fat depot. Incubations with isoproterenol (10 microM) and dibutyryl-cAMP (2.5 mM) both reduced estradiol binding by 56% (P less than 0.005), while insulin (1 nM) enhanced the estradiol binding by 37% (P less than 0.01). In conclusion, a specific and high affinity nuclear estradiol receptor was demonstrated in rat adipocytes and regional differences in nuclear estradiol binding were detected. Furthermore, it was demonstrated that nuclear estradiol binding could be modulated by other agents known to affect adipocyte metabolism.
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PMID:Nuclear estradiol binding in rat adipocytes. Regional variations and regulatory influences of hormones. 164 50

Male Sprague-Dawley rats displayed significantly higher rates of triglyceride/fatty acid (TG/FFA) substrate cycling in subcutaneous, perigenital, and mesenteric white adipose tissue, compared to females. To investigate possible regulation via androgens and estrogens, male rats were treated with the androgen antagonist, cyproterone acetate (10 mg daily in subcutaneous injections), or estradiol polyphosphate (0.3 mg intramuscularly, given as a single dose). Estradiol treatment did not affect TG/FFA cycling. Treatment with cyproterone acetate significantly decreased TG/FFA cycling in perigenital (epididymal) tissue. This effect could however largely be ascribed to concomitant inhibition of food intake by cyproterone acetate. The effects of cyproterone acetate on the two axes of TG/FFA cycling (lipolysis and re-esterification) were further studied in vitro. Norepinephrine-stimulated glycerol release from perigenital adipocytes was inhibited, whereas activities of esterification enzymes (GPAT and PPH) was essentially unaffected. We conclude that androgens seem to affect TG/FFA cycling indirectly via the lipolytic axis.
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PMID:Sex difference in triglyceride/fatty acid substrate cycling of rat adipose tissue: indirect regulation by androgens. 183 7

To obtain evidence of a physiological role for androgens and estrogens in the regulation of the epididymis of sexually immature rabbits, the effects of these hormones on [35S] methionine incorporation into epididymal proteins in vitro were examined. Two-dimensional polyacrylamide gel electrophoresis revealed that short term incubation with estradiol changed the patterns of radiolabeled proteins detected in tissue homogenates of epididymal segments from castrated rabbits compared to those in segments from castrated rabbits that were not exposed to exogenous estradiol. Most of the changes seen in corpus tissue affected proteins with a wide range of pI values and relatively high mol wt (greater than 40K). The effects on caput and cauda tissue proteins were seen over a wide pH and mol wt range. Castration abolished many of the regional differences in protein synthesis; these were restored by incubation with estradiol. Testosterone had little effect on the synthesis of tissue proteins, except for stimulation of the synthesis of a single protein (17K; pI 5.1) in all three segments and stimulation of a small group of proteins (less than 14K; pI 7.0-7.2) in the corpus. Estradiol had little effect on proteins secreted by epididymal segments. Testosterone, however, stimulated the synthesis of a number of unique proteins secreted by the caput and corpus and resulted in a pattern of radiolabeled proteins similar to that obtained with intact animals. Additional secretory proteins could be stimulated in caput, but not corpus, tissue minces from intact rabbits by exogenous testosterone. No androgen-specific synthesis of secretory proteins was detected in the cauda of either castrated or intact rabbits. Estradiol affected the synthesis of both secreted and tissue proteins in terms of influencing which epididymal segment was most active at incorporating [35S]methionine into radiolabeled proteins and which was least active. Testosterone had a similar influence on secreted proteins, but did not have any analogous effect on tissue proteins. These results indicate that testosterone and estradiol influence the synthesis of proteins by the immature rabbit epididymis and that both may, therefore, be important physiological regulators of epididymal development and/or function.
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PMID:Estrogen and androgen regulation of protein synthesis by the immature rabbit epididymis. 273 45

We measured the 5 alpha-reductase activity in isolated cell preparations of rat adipose tissue using the formation of [3H]dihydrotestosterone from [3H]testosterone as an endpoint. Stromal cells were prepared from the epididymal fat pad, perinephric fat, and subcutaneous fat of male rats and from perinephric fat of female rats. Adipocytes were prepared from the epididymal fat pad and perinephric fat of male rats. Stromal cells from the epididymal fat pad and perinephric fat contained greater 5 alpha-reductase activity than did the adipocytes from these depots. Stromal cells from the epididymal fat pad contained greater activity than those from perinephric and subcutaneous depots. Perinephric stromal cells from female rats were slightly more active than those from male rats. Estradiol (10(-8) M), when added to the medium, caused a 90% decrease in 5 alpha-reductase activity. Aromatase activity was minimal, several orders of magnitude less than 5 alpha-reductase activity in each tissue studied.
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PMID:5 alpha-reductase activity in rat adipose tissue. 367 52

The possible physiological role of estrogen in the epididymis and ventral prostate of rat was investigated. In prepubertal rats castrated for 7 days, treatment with estradiol (1.0 micrograms) for 7 days (35-day-old at autopsy) resulted in a marked increase in the weight and content of glyceryl-phosphorylcholine and sialic acid in the epididymis; estradiol and dihydrotestosterone were equipotent in causing an increase in sialic acid concentration. Estradiol showed a synergistic effect in influencing the androgen action on the growth of the prepubertal rat prostate while no such synergism was evident in stimulating the secretory function of the epididymis. The duality of epididymal response to the two sex steroids suggests that the two hormones may be acting in concert at physiological levels as regulators of epididymal secretory function; the need for identifying estrogen specific biochemical indices in the epididymis is discussed.
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PMID:Biological response of the rat epididymis to estrogen. 378 Aug 62

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

Polychlorinated biphenyls (PCBs) have been reported to adversely affect reproduction in laboratory and wild animals. The present study was undertaken to determine the toxic potential of Aroclor-1254 (A-1254) on in vitro fertilizing ability of oocytes and epididymal sperm and on preimplantation embryo development in the mouse. A-1254 was added to the IVF medium at concentrations of 0.01, 0.1, 1.0, and 10.0 micrograms/mL. Cumulus masses containing the oocytes were obtained from superovulated B6D2F1 mice and were placed in the culture medium containing A-1254 to which epididymal sperm, capacitated in a medium without A-1254, were added. The IVF rate was assessed 20 to 24 h after insemination. A-1254 significantly reduced the mean percent ova fertilized even at 0.1 microgram/mL. Incubation of the cumulus masses in various concentrations of A-1254 for 6 h, followed by insemination with sperm capacitated in the presence of A-1254, also significantly reduced the IVF rate. Capacitation of sperm in A-1254-containing medium, followed by coculture with untreated oocytes, failed to affect the IVF rate. No significant effect on sperm motility was observed following exposure to 1 and 10 micrograms/mL of A-1254. Estradiol-17 beta also reduced the IVF rate, however, the effect of A-1254 was more severe compared to the estradiol treatment. Furthermore, addition of A-1254 to the embryo culture medium was associated with a significant decrease in embryo growth at 48 h and 96 h. These results demonstrate adverse effects of A-1254 on oocytes, IVF, and embryonic development in the mouse.
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PMID:Reproductive toxicity of Aroclor-1254: effects on oocyte, spermatozoa, in vitro fertilization, and embryo development in the mouse. 856 93

The difference between in vivo and in vitro inhibitory effects on epididymal 5 alpha-reductase was investigated by using epididymides obtained from patients treated with chlormadinone acetate (6-chloro-3,20-dioxo-4,6-pregnadien-17-yl acetate, CMA) or ethinylestradiol (17 alpha-ethynyl-1,3,5(10)-estratriene-3,17 beta-diol, EE2). In the in vitro study CMA exhibited competitive inhibition, whereas EE2 was a noncompetitive inhibitor of human epididymal 5 alpha-reductase. Their in vitro inhibitory effects were weak compared with the effect of finasteride ((-)-N-tert-butyl-3-oxo-4-aza-5 alpha-androst-1-ene-17 beta carboxamide), a steroidal 5 alpha-reductase inhibitor. The Ki values of CMA, EE2, and finasteride were 1.4 x 10(-5) M, 1.5 x 10(-5) M, and 1.3 x 10(-9) M, respectively. Despite their weak in vitro inhibitory potency, CMA and EE2 strongly inhibited testosterone 5 alpha-reductase in vivo. There were regional differences in inhibitions by CMA and EE2 on human epididymal 5 alpha-reductase activity depending on the site of the epididymis; the efferent ductules, the head, the body or the tail. In vivo administration of CMA reduced epididymal 5 alpha-reductase activity by 49.7% to 89.4%. In vivo administration of EE2 reduced epididymal 5 alpha-reductase activity by 82.7% to 96.3%. The apparent Km values for the enzyme in patients treated with CMA or EE2 and untreated patients did not differ significantly. The Vmax values were significantly decreased in treated patients. These findings suggest that the marked in vivo inhibition of 5 alpha-reductase induced by CMA and EE2 was not related to the direct action of these compounds, but resulted from a reduction in the amount of the enzyme.
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PMID:Effects of chlormadinone acetate and ethinylestradiol treatment on epididymal 5 alpha-reductase activities in patients with prostate cancer. 915 25

This study was designed to determine if long-term exposure to high doses of methoxychlor (M) would alter pituitary or testicular endocrine functions in either an estrogenic or antiandrogenic manner. Weanling male Long-Evans hooded rats were dosed daily with M (po) at 0, 200, 300, or 400 mg kg-1 day-1 for 10 months. Methoxychlor treatment delayed puberty by as much as 10 weeks and reduced fertility and copulatory plug formation in a dose-related manner at the initial mating. During mating, M-treated males exhibited shorter latencies to mount and ejaculate versus control males, but the number of intromissions prior to ejaculation was unaffected, indicating that M enhanced the arousal level in the males in an estrogen-dependent manner. Most treated males eventually mated but time-to-pregnancy was lengthened. Very low sperm counts were associated with infertility, while prolonged delays in puberty reduced fecundity. Methoxychlor treatment with 200 to 400 mg kg-1 day-1 failed to mimic the chronic effects of a sustained (8 months) low dose of estradiol-17 beta (3-mm silastic implants) on pituitary or testicular hormone levels. Estradiol administration increased pituitary weight 4-fold, serum levels of luteinizing hormone (LH) were reduced by almost 50%, and serum prolactin was increased 40-fold, while M did not affect any of these measures. These data demonstrate that M affects the CNS, epididymal sperm numbers, and the accessory sex glands and delays mating without significantly affecting the secretion of LH, prolactin, or testosterone. These data indicate that M did not alter pituitary endocrine function in either an estrogenic or antiandrogenic manner. To our knowledge, these data provide the first in vivo example of such a pronounced degree of target tissue selectivity to an environmental endocrine-disrupting chemical.
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PMID:The estrogenic and antiandrogenic pesticide methoxychlor alters the reproductive tract and behavior without affecting pituitary size or LH and prolactin secretion in male rats. 1018 90


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