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 incorporation of radioactivity into various cells in the sequence of spermatogenesis was measured by preparing highly purified spermatozoan nuclei from the cauda epididymidis of mice at daily intervals after injection of (3H)thymidine. The stages of differentiation of these sperm at the time of thymidine administration were calculated from the kinetics of spermatogenesis. The procedure for purification of sperm nuclei included sonication, mechanical shearing, and treatment with trypsin, DNase, Triton X-100, 2M NaC1, and sodium dodecyl sulfate. DNA was isolated from these nuclei by treatment with dithiothreitol and pronase, followed by phenol extraction and ethanol precipitation. The levels of radioactivity in the epididymal sperm head preparations were low (less than 13 dpm/mouse) for 27 days after injection, and then rose dramatically to over 4 times 104 dpm/mouse. Further experiments demonstrated that the 11 dpm of 3H radioactivity contained in sperm heads at 21 or 26 days after injection of (3H)TdR was significantly above background and contamination levels from other cells or other sources. Most of the radioactivity was in the sperm DNA and represented incorporation of tritium from (3H)TdR into the nuclear DNA of meiotic cells at 0.002 percent of the rate of incorporation into S-phase cells. Little, if any, (3H)TdR was incorporation into the DNA of spermatids. The levels of DNA synthesis during the meiotic prophase in the mouse appear to be much lower than those reported for other organisms.
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PMID:Meiotic DNA synthesis during mouse spermatogenesis. 110 31

Single oral doses of the haemorrhagic antioxidant 2,4,6-tri-t-butylphenol (260 mg/kg) were well absorbed in the rat. Peak blood levels of this compound were reached in 15-60 min. The blood elimination half-lives were 18.2 min for the alpha-phase and 11.8 h for the slower beta-phase. Max. tissue concns. of this compound were reached 2-3 h in the liver, 2-6 h in kidneys, 1.5-2.5 h in spleen and greater than 24 h in epididymal adipose tissues. This compound and its metabolites were not excreted in the urine; a metabolite but not the parent compound was detected in the faeces. The faecal metabolite had a mol. wt. of 261, and was considered to be 2,4,6-tri-t-butylphenoxy radical. 2,4,6-Tri-t-butylphenoxy radical was also detected in the bile of rats after oral administration of the parent phenol.
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PMID:Metabolic studies in the rat with 2,4,6-tri-t-butylphenol: a haemorrhagic antioxidant structurally related to butylated hydroxytoluene. 663 29

The effects of A(2) adenosine receptor agonists upon phenylephrine-stimulated contractility in preparations of rat epididymis were investigated. Preparations responded to phenylephrine (3 microM) with submaximal contractions. Adenosine and the stable agonists 5'-N-ethylcarboxamido-adenosine (NECA) and 2-p-(2-carboxyethyl) phenethylamino-N-ethylcarboxamide adenosine (CGS 21680) inhibited phenylephrine-induced contractions (potency order, NECA>CGS 21680>adenosine). The A(2A) receptor-selective antagonist, 4-(2-[7-amino-2-(2-furyl)[1,2,4]-triazolo-[2,3-a][1,3, 5]triazin-5-ylamino]ethyl)phenol (ZM 241385, 30 microM) blocked the response to NECA. The A(2A) adenosine receptor-mediated inhibitory responses to NECA were reduced by the K(ATP) channel blocker, glibenclamide (3 microM) and abolished by charybdotoxin (100 nM). The diterpene forskolin elicited a concentration-dependent inhibition of phenylephrine (3 microM)-stimulated contractility (by 62+/-8% of control at 100 microM). Charybdotoxin (100 nM), but not glibenclamide (3 microM) blocked the forskolin (10 microM) inhibition of phenylephrine-stimulated contractility. NECA elicited concentration-dependent increases in both cyclic AMP and cyclic GMP accumulation which were antagonized by ZM 241385 (30 nM). The protein kinase G activator, APT-cyclic GMP (8-(-Aminophenylthio) guanosine-3',5'-cyclic monophosphate) and the protein kinase A activator (Sp)-8-bromoadenosine-3',5'-cyclic monophosphorothioate (Sp-8-Br-cyclic AMPs), inhibited phenylephrine (3 microM) induced contractions of rat epididymis. Glibenclamide (3 microM), but not charybdotoxin (100 nM), inhibited ATP-cyclic GMP responses. Charybdotoxin (100 nM), but not glibenclamide (3 microM) reduced the effect of Sp-8-Br-cyclic AMPs. This study shows that the A(2A) adenosine receptor inhibition of epididymal contractility may be mediated through the activation of charybdotoxin- and glibenclamide-sensitive potassium channels and may involve the activation of both protein kinases A and G.
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PMID:A(2A) adenosine receptor mediated potassium channel activation in rat epididymal smooth muscle. 1082 99

We evaluated sequelae to early exposure of male rabbits to drinking water containing chemicals typical of ground water near hazardous waste sites. The mixture (p.p.m. at 1x) was 7.75 arsenic, 1.75 chromium, 9.25 lead, 12.5 benzene, 3.75 chloroform, 8.5 phenol and 9.5 trichloroethylene. Dutch-Belted does received mixture at 0x (deionized water; control), 1x or 3x as drinking water from day 20 pregnancy through weaning. Exposure of individual males (7-9/treatment) continued until 15 weeks (adolescence); then, all males received deionized water. At 57-61 weeks of age, ejaculatory capability and seminal, testicular, epididymal and endocrine characteristics were evaluated. At 10 opportunities with a female teaser, all seven control males ejaculated every time, but 12 of the 17 treated males failed to express interest, achieve erection and/or ejaculate on one to five occasions; four of the 12 accomplished ejaculation with a second male teaser. Total spermatozoa/ejaculate and daily sperm production were unaffected. However, treatment caused (P < 0.03) acrosomal dysgenesis and nuclear malformations. Baseline serum concentrations of LH were lower, but with borderline significance (P = 0.05). Testosterone secretion after exogenous human chorionic gonadotrophin (P < 0.04) was low. Thus, even at 45 weeks after last exposure to drinking water pollutants, mating desire/ability, sperm quality, and Leydig cell function were subnormal.
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PMID:Long-term effects on male reproduction of early exposure to common chemical contaminants in drinking water. 1133 49

The adenosine-receptor modulation of noradrenaline release was compared in prostatic and epididymal portions of rat vas deferens. In both portions, tritium overflow elicited by electrical stimulation (100 pulses/8 Hz) was reduced by the adenosine A(1) receptor agonist, N(6)-cyclopentyladenosine, and enhanced by the nonselective receptor agonist, 5'-N-ethylcarboxamidoadenosine, in the presence of the adenosine A(1) receptor antagonist, 1,3-dipropyl-8-cyclopentyl-1,3-dipropylxanthine (DPCPX; 20 and 100 nM). The adenosine A(2A) receptor agonist, 2-p-(2-carboxyethyl)phenethyl-amino-5'-N-ethylcarboxamidoadenosine, increased tritium overflow, but only in the epididymal portion. The enhancement caused by NECA was prevented by the adenosine A(2A) receptor antagonist, 4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo-[2,3-a][1,3,5]triazin-5-ylamino]ethyl)phenol (ZM 241385; 20 nM), in the epididymal and by the adenosine A(2B) receptor antagonist, alloxazine (1 microM), in the prostatic portion. Inhibition of adenosine uptake enhanced tritium overflow in both portions, an effect blocked by ZM 241385 in the epididymal and by alloxazine in the prostatic portion. The results indicate that adenosine exerts an adenosine A(1) receptor-mediated inhibition, in both portions, and facilitation mediated by adenosine A(2A) receptors in the epididymal and by A(2B) receptors in the prostatic portion.
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PMID:Facilitation of noradrenaline release by adenosine A(2A) receptors in the epididymal portion and adenosine A(2B) receptors in the prostatic portion of the rat vas deferens. 1212 70

Operating time for idiopathic hydroceles and epididymal cysts is scarce as these conditions compete with an increasing caseload of more consequential surgical disease. Therapy is often relegated to repeated aspiration. Sclerotherapy appears to be effective in a majority of published trials, but comparative effectiveness, efficacy and safety of most agents, including phenol versus tetracycline, has not been established A deliberate strategy of re-treatment until cure is not universally practised, with surgery still being offered after single-treatment failures. Two trials, the first consisting of 53 scrotal cysts treated with 5% phenol-in-water and the second, 42 cysts treated with tetracycline, are compared for effectiveness, efficacy and safety of sclerotherapy per se and of re-treatment. Intention-to-treat analysis yields similar cure rates (no re-accumulation three months after last injection) for phenol and tetracycline (83% and 81% respectively, p = 0.8). Per-protocol analysis also yields similar cure rates (100% and 97% respectively, p = 0.26) and mean number of injections to cure (1.34 and 1.12 respectively, p = 0.069), with range 1-4 and 1-3 respectively. Severe pain following tetracycline injection required administration of pre-injection cord block. Other complications occurred equally (25% and 25.7% respectively, p = 0.94) and were trivial except for one case of chronic haematocele treated by orchiectomy in the tetracycline group. Phenol (5%) and tetracycline are equally efficacious sclerosants for idiopathic scrotal cysts, achieving almost 100% cure with re-treatment and matching the efficacy of surgery. Concern about post-treatment fertility applies equally to surgery and demands informed consent for both modalities.
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PMID:Sclerotherapy of idiopathic hydroceles and epididymal cysts: a historical comparison trial of 5% phenol versus tetracycline. 1864 96