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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 epididymal and testicular fluids on the fertilizing capacity of spermatozoa were observed in New Zealand white rabbits before they entered the epidiymis and after passage through it. Techniques employed are described. Spermatozoa were collected from the rete testis and from the cauda epididymis and mixed with fluids from these 2 sites. In all cases spermatozoa in .15 ml of Hanks balanced salt solution were instilled into each uterine horn of rabbits concurrently given 50 IU of human chorionic gonadotropin (HCG). 26-28 hours later recovered eggs were checked with phase contrast microscopy for evidence of fertilization. Spermatozoa taken from the distal cauda epididymis were fertile immediately after collection. After moderate centrifugation and resuspension of these spermatozoa in epididymal or testicular fluid fertility was retained. Testicular spermatozoa were infertile in all experiments. In in vitro tests, using fluid from the rete testis, the fertility of spermatozoa from the cauda epididymis was retained. Fluid from the cauda epididymis failed to induce fertility in testicular spermatozoa. Results suggest that there may be a time-dependent process involved in the capacitation of spermatozoa rather than a fluid contact effect. However, it is also possible that spermatozoa may need to come in contact with secretions of the corpus epididymis to become fertile.
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PMID:The effect of epididymal and testicular fluids on the fertilising capacity of testicular and epididymal spermatozoa. 119 May 8

The objectives of the study were to determine whether a low dose of a luteinizing hormone-releasing hormone analogue (buserelin) has an effect on testicular descent, if buserelin affects germ cell maturation and epididymal development, the incidence of retractile testes in the controlled trials, and if the subsequent administration of human chorionic gonadotropin has any effect on the groups treated. The study was double blind, placebo controlled in which patients with cryptorchidism were assigned randomly into 3 groups: buserelin treatment (22), surgical treatment (18) or placebo control group (19). The 3 groups of patients were similar before treatment in regard to testicular position, chronological and bone age, height and weight, luteinizing hormone, follicle-stimulating hormone, testosterone, penile size and the volume of the contralateral testis. Buserelin (20 micrograms). administered daily in a nasal spray significantly induced testicular descent compared to the group treated with a placebo (p less than 0.01). A normal epididymis was found more often in boys with successful descent (p less than 0.003). Boys treated with buserelin had the highest number and the best maturation index of the germ cells; human chorionic gonadotropin influenced the descent in both groups but it was more efficacious when it was administered after treatment with buserelin, although it had no additional effect on germ cell maturation. None of the boys had retractile testes. Buserelin was capable of inducing testicular descent in addition to increasing simultaneously the number of germ cells and provoking further development of the epididymis.
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PMID:Buserelin treatment of cryptorchidism: a randomized, double-blind, placebo-controlled study. 135 40

Human chorionic gonadotropin, kallikrein, indomethacin, and hydralazine were administered to different groups of varicocelized rats, while surgical repair of the varicocele was performed in another group of rats. The effects of conservative and surgical treatment on epididymal sperm content and motility, the weights of the testes, epididymis, and male accessory genital glands, and fertility were compared between each group and a sham-treated group of rats. Surgical repair significantly improved all the evaluated parameters and all the conservative regimens, except hydralazine, resulted in a significant improvement in most parameters. Our results indicate that stimulation of the Leydig or/and Sertoli cells of a varicocelized testicle can counteract some of the detrimental consequences of the varicocele itself.
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PMID:Surgical repair versus medical treatment of varicocele in the rat: pharmacological manipulation of the varicocelized testicle. 142 45

We have shown earlier that the administration of cyclosporine impairs testicular function and causes a decrease in sperm counts, sperm motility and fertility. In order to determine whether or not the deleterious effects of CsA could be reversed by hormonal therapy, we injected sexually mature male Sprague Dawley rats with cremaphor + saline or CsA (40 mg./kg./d) alone or in combination with human chorionic gonadotropin (hCG; five micrograms./d/rat) and follicle stimulating hormone (FSH; five micrograms./d/rat). The injections were given subcutaneously for 14 days. As expected, CsA administration decreased the body and reproductive organ weights, testicular and epididymal sperm counts, sperm motility and fertilizing ability. Serum levels of LH were elevated and testosterone was decreased. The administration of FSH + hCG to the CsA treated rats restored the body and reproductive organ weights, sperm counts and motility. Seventy five percent of gonadotropin treated males were fertile as compared to 25% in the CsA treated group. In the hormone treated group, the blood levels of CsA were 50% of that of CsA treated group. In order to verify whether or not the decline in the blood levels of CsA was the cause for the amelioration of CsA-induced changes in the reproductive function, we compared the CsA + hormone treated group with another group treated with five mg./kg./d CsA which had blood levels of CsA comparable to the former group. In the five mg./kg./d group the reproductive functions were significantly lower than the CsA + hormone treated group suggesting, therefore, that the restoration of reproductive functions in the CsA + hormone treated group is a result of hormonal treatment. Administration of CsA (40 mg./kg./d) reduced the kidney weight and increased the levels of serum creatinine: these changes were also ameliorated by the administration of hCG + FSH.
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PMID:Reversal of the toxic effects of cyclosporine on male reproduction and kidney function of rats by simultaneous administration of hCG + FSH. 212 12

Administration of cyclosporine to rats has been shown to impair testicular function, resulting in a decrease in sperm counts and fertility. In order to determine whether or not the deleterious effects of CsA could be reversed by hormonal therapy, mature male Sprague Dawley rats were treated with CsA (40 mg/kg/day, s.c.) alone or in combination with human chorionic gonadotropin (hCG) (5 micrograms/day/r; s.c.) for 14 days. Cyclosporine administration decreased the body weight (290 +/- 5.30 vs. 339 +/- 8.7 g; P less than 0.05) and reproductive organ weights (testis 1.49 +/- 0.42 vs. 1.60 +/- 0.03 g; epididymis 0.41 +/- 0.02 vs. 0.49 +/- 0.002 g; seminal vesicle 0.61 +/- 0.09 vs. 1.60 +/- 0.05 g; prostate 0.28 +/- 0.04 vs. 0.60 +/- 0.06 g; P less than 0.05) testicular sperm counts (5.80 +/- 0.42 vs. 8.49 +/- 0.48 x 10(7)/100 mg tissue; P less than 0.05) and epididymal sperm counts, (28.2 +/- 0.95 vs. 51 51.62 +/- 2.17 x 10(7)/100 mg tissue; P less than 0.05) and fertility (25% vs. 100%). Serum levels of LH were elevated (101.98 +/- 21.48 vs. 25.6 +/- 5.18 ng/ml; P less than 0.05) and testosterone was decreased (0.48 +/- 0.07 vs. 2.06 +/- 0.56 ng/ml; P less than 0.05). The administration of hCG to the CsA-treated rats restored the reproductive organ weights (testis 1.56 +/- 0.043 g; seminal vesicle 1.04 +/- 0.05 g; prostate 0.70 +/- 0.06 g) and sperm counts (testicular 7.88 +/- 1.0 x 10(7)/100 mg tissue; epididymal 59.86 +/- 4.16 x 10(7)/100 mg tissue; P less than 0.05) Serum levels of testosterone (18.63 +/- 4.45 ng/ml) and LH (431.65 +/- 31.41 ng/ml) were significantly elevated, as compared with control and CsA-treated groups (P less than 0.05). All the rats in the gonadotropin-treated group were fertile, as compared with 25% in the CsA-treated group. CsA reduced the kidney weight (1.17 +/- 0.02 vs. 1.27 +/- 0.03 g; P less than 0.05) and increased the levels of serum creatinine (0.97 +/- 0.07 vs. 0.59 +/- 0.03 mg/dl; P less than 0.05): these changes were ameliorated by the administration of hCG (kidney weight 1.35 +/- 0.03 g; creatinine 0.76 +/- 0.09 mg/dl).
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PMID:Evaluation of the effect of experimental cyclosporine toxicity on male reproduction and renal function. Reversal by concomitant human chorionic gonadotropin administration. 230 Oct 8

Prolactin (PRL) binds to the testis of mice and rats where it increases the number of luteinizing hormone receptors, increases the binding of human chorionic gonadotropin (hCG) to LH receptors, and enhances testosterone synthesis and secretion. PRL also binds to the prostate and seminal vesicles of rats and humans where it increases organ weight and stimulates growth and uptake of testosterone. PRL binds to the epididymis of rats but the effect of PRL on this organ is unknown. In the present study, a standard immunoperoxidase (PAP) technique was used to detect the binding of endogenous and exogenous PRL or PRL-like peptides to the epididymis of the mature mouse. Throughout the epididymal duct, a positive reaction for peroxidase, suggesting PRL or PRL-like binding, occurred in the Golgi area of principal cells. In segment 1, positive reactions were also visualized in the perinuclear area and in the region located between the Golgi area and the apical surface of the principal cells (supra-Golgi area). In the corpus and cauda epididymidis, scattered entire principal cells were also positive. Throughout the epididymal duct, the reactions indicating the binding of exogenous PRL were slightly stronger than those testing for binding of endogenous peptides. The significance of such binding to the epididymis is uncertain but PRL may perform the same functions in epididymal principal cells as it does in the testis, prostate, and seminal vesicles.
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PMID:Immunocytochemical detection of prolactin or prolactin-like immunoreactivity in epididymis of mature male mouse. 231 57

This paper compares the statistical precision and biological sensitivity of multiple indices of reproductive function to infertility in the male rodent. The studies discussed include those that examined reproductive function in the male following perinatal exposure to reproductive toxicants and others in which the compounds were administered to young-adult males, often with very diverse results. For example, some chemicals that alter sex differentiation reduce fertility by affecting breeding performance alone (polychlorinated biphenyls (PCBs), fenarimol, or losulazine), without altering sperm and testicular measures. Others also markedly alter sex differentiation of the genitalia, the accessory glands and the testis in addition to their effects on central nervous system (CNS) sex differentiation and mating behavior (testosterone, flutamide, cyproterone acetate, tamoxifen, estradiol and diethylstilbestrol (DES)). In contrast, prenatal exposure to compounds that alter primary germ cell survival (busulphan, congo red) induce partial gonadal/germ cell agenesis without altering sex differentiation. These chemicals dramatically reduce testicular sperm production in the male offspring, and the most severely affected males are infertile. In a series of studies conducted in our laboratory, young male rats were exposed to known reproductive toxicants in a dose related manner from puberty, through young adulthood and breeding. We have found that the profile of effects varies considerably depending upon the chemical's mechanism of toxicity. When a compound produced infertility through direct effects of testicular function (Carbendazim (MBC) and dibutyl phthalate (DBP)), then testis weight, testicular histology, and testicular sperm head counts provided sensitive indicators of toxicity. In general, dramatic reductions in sperm production are required to induce infertility and these changes were accompanied by elevated serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) and changes in human chorionic gonadotropin (hCG)-stimulated testosterone synthesis. Chemicals that have hormonal activity, alter the internal endocrine environment, or directly effect CNS function induce a completely different profile of effects. For example, estrogen administration alters the function of the seminal vesicle and the endocrine system, and reduces epididymal sperm reserves; while testicular measures are relatively unaffected. Since very different spectrums of effects are produced by different compounds, no single endpoint will consistently be the most sensitive indicator of reproductive toxicity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Correlation of sperm and endocrine measures with reproductive success in rodents. 266 89

In the present study rats were dosed from weaning, through puberty and gestation, to Day 15 of lactation with methoxychlor at 25, 50, 100, or 200 mg/kg/day. Morphological landmarks of puberty were measured, including the ages at vaginal opening, first estrus, and first estrous cycle in females and at preputial separation in males. In the female, estrous cyclicity, fertility, litter size, number of implantation sites, organ weights, and ovarian and uterine histology were also measured. The viability of the offspring (F1) and their fertility were evaluated using a continuous breeding protocol. Males were necropsied after breeding, the reproductive organs were weighed, and the cauda epididymal sperm counts were determined. One testis was used for histopathology, while the other was used to quantify interstitial fluid (IF) content, IF testosterone concentration, and testicular sperm production. Testosterone and androgen-binding protein were measured in the caput epididymis, and sperm motility and morphology were evaluated from a caudal sample. The serum and pituitary were saved for hormonal determinations. Methoxychlor accelerated the age at vaginal opening and first estrus, and the vaginal smears were cornified. Growth was retarded at 100 and 200 mg/kg/day and fertility was reduced when the females were bred with untreated or similarly treated males. In the highest-dose group, the mated females went from constant estrus into pseudopregnancy following mating, but they had no implants. In males, methoxychlor treatment markedly reduced growth, seminal vesicle weight, cauda epididymal weight, caudal sperm content, and pituitary weight. Puberty was delayed in the two highest-dosage groups. Testicular sperm measures were much less affected than caudal measures. Testis weight and histology were slightly affected, and testicular sperm production, sperm morphology, and motility were unaffected. Endocrine function of the testes and pituitary was altered by methoxychlor administration. Leydig cell testosterone production, in response to human chorionic gonadotropin challenge, was reduced and pituitary levels of prolactin, thyroid-stimulating hormone (TSH), and follicle-stimulating hormone (FSH) were altered. In contrast, serum levels of prolactin, FSH, and luteinizing hormone were unaffected. Serum TSH was reduced by 50% of control at 100 and 200 mg/kg/day, while pituitary levels were increased. Gonadotropin-releasing hormone concentration in the mediobasal hypothalamus was also elevated. In spite of the many reproductive alterations, the fertility of treated males was not reduced when they were mated with untreated females.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:A dose-response analysis of methoxychlor-induced alterations of reproductive development and function in the rat. 292 22

This is a retrospective review of 62 patients with Stage II testicular seminoma treated either by initial radiation therapy (48 patients) or by platinum-containing chemotherapy (14 patients). For all 62 cases, disease-free survival from 2 to 20 years was 86%, uncorrected survival was 86% at 5 years and 83% at 15 years, and survival corrected for deaths from intercurrent disease was 90% from 2 to 20 years. There were no significant differences in outcome between the two treatment groups. An analysis of potential prognostic factors for the initial radiation therapy group and for the whole group revealed that age, site of primary, cryptorchidism, ipsilateral hernia repair, contralateral testicular atrophy, scrotal incision, elevated postorchiectomy beta-human chorionic gonadotropin level, epididymal invasion, spermatic cord involvement, and vascular invasion in the primary were not significant. However, bulk of abdominal disease was a prognostic factor. Patients with small-volume abdominal disease defined as nonpalpable disease or as a mass less than 10 cm in largest diameter accounted for two-thirds of the series and had a disease-free survival of 95% when treated with initial radiation therapy. Patients with bulky disease, either palpable or greater than or equal to 10 cm in diameter, had a disease-free survival of 64%. The relative roles of the two treatments in bulky abdominal disease are discussed, but in the absence of a prospective study it is not possible to definitively answer the question of which modality is best in this setting. In our series, the patients treated with platinum-containing chemotherapy fared as well as the primarily irradiated patients, but 71% of the former had palpable masses, compared with 22% of the latter. The chemotherapy-treated patients who relapsed were treated with radiation therapy for salvage, leading to a 100% survival corrected for intercurrent death. We have therefore elected to continue the policy of initial radiation therapy for small-volume (less than 10 cm) disease and platinum-containing chemotherapy for bulky disease (greater than or equal to 10 cm), with irradiation used for residual masses.
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PMID:The role of radiation in stage II testicular seminoma. 381 84

Carnitine and its short-chain acyl esters were assayed in semen from normospermic and azoospermic men. Extremely low concentrations of free carnitine and acylcarnitine were found in semen from patients with obstructive azoospermia where the ejaculate was primarily of prostatis origin, and low values were also obtained in obstruction of the vas deferens, where the epididymal contents were not ejaculated. Semen from patients whose azoospermia was caused by testicular dysfunction had low acylcarnitine concentrations and normal levels of free carnitine in most cases, but a group of patients with severe testicular failure (including cases of Klinefelter syndrome and cryptorchidism) had low semen free carnitine concentrations. Whereas treatment with human chorionic gonadotropin increased serum testosterone levels in azoospermic patients, it did not increase the free carnitine concentration in semen, although it increased the proportion of carnitine found in acylcarnitines.
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PMID:Carnitine and acylcarnitines in semen from azoospermic patients. 611 78


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