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)

This study examines the effects of a potent gonadotropin releasing hormone (GnRH)-antagonist (GnRH-A, Ac-D[2] Nal1, 4-CL-D Phe2, D-Trp3, D-Arg6, D-Ala10) upon the distribution of androgen binding protein (ABP) in serum, testis, and epididymis, and its relationship with the completion of spermatogenesis in Sprague-Dawley rats. After 2 weeks of daily injections of 10 micrograms/kg, 50 micrograms/kg, 100 micrograms/kg, or 500 micrograms/kg of GnRH-A, testicular ABP content was either unchanged or elevated (P less than 0.05), and serum ABP levels were elevated (P less than 0.01). Spermatogenesis was maintained in animals administered 10 micrograms/kg or 50 micrograms/kg GnRH-A, and epididymal ABP content remained unchanged. On the other hand, daily injections of 100 micrograms/kg or 500 micrograms/kg GnRH-A resulted in a significant decrease in epididymal ABP content (P less than 0.05), and spermatogenesis was arrested at early spermiogenesis. After 4 weeks of GnRH-A administration, both testicular and epididymal ABP were decreased in a dose-dependent manner in animals receiving doses of 50 micrograms/kg or higher of GnRH-A. In order to evaluate the normalcy of the bidirectional release of ABP in GnRH-A treated rats, additional rats were given daily injections of 25 micrograms/kg or 250 micrograms/kg of GnRH-A for 2 weeks. Concentrations of ABP in interstitial fluid (ITF) and seminiferous tubular fluid (STF) remained unchanged, but serum ABP levels were significantly increased (P less than 0.05) in rats administered 25 micrograms/kg GnRH-A. Qualitatively normal spermatogenesis was maintained and epididymal ABP content did not differ from that of control animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:GnRH-A induced arrest of spermiogenesis in rats is associated with altered androgen binding protein distribution in the testis and epididymis. 159 99

Three male dogs, aged 2-4 years, which exhibited a high percentage of sperm with abnormal tails in their semen and low levels of peripheral plasma LH and testosterone were given two injections of 400 micrograms an LHRH analogue (LHRH-A) 3 h apart. The semen quality of all three dogs and the peripheral plasma levels of LH and testosterone were examined in two of the dogs. Plasma levels of LH and testosterone in both dogs peaked at 30 and 90 min respectively, after the injection of LHRH-A. The semen quality of all three dogs had improved temporarily 20 days after the injection. To be specific, although the mean percentage of sperm with abnormal tails in the three dogs was 19, 26 and 32% respectively before injection of LHRH-A, these values had decreased to 10, 16 and 13%, respectively, 20-40 days later. Thereafter, however, the percentage sperm abnormalities increased again. The testes and epididymides of two of the dogs were examined histologically at the end of 90 days. Sloughed germ cells were observed in the seminiferous tubules of the testes, and pyknotic epithelial cells were noted in some of the epididymal ducts. The other dog, which had a history of three unsuccessful matings was treated again with LHRH-A and mated with three bitches 30, 75, and 110 days later, respectively. Only the bitch mated with this dog 30 days after a second series of injections conceived. It is assumed that the semen quality of the three dogs improved because of a temporary rise in plasma LH and testosterone levels after the injection of LHRH-A. It is concluded that the fertility of dogs with a high percentage of sperm with abnormal tails can be improved approximately 30 days after treatment with an LHRH-A.
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PMID:Effects of LHRH-analogue treatment of spermatogenic dysfunction in the dog. 176 24

A method of direct percutaneous injection of testosterone (T)-laden microspheres directly into the testis was used in an attempt to achieve the maintenance of normal intratesticular T concentrations, spermatogenesis, and fertility. Rats were divided into three groups: (1) sham operated/injection controls; (2) animals receiving 250 micrograms/d gonadotropin-releasing hormone (GnRH)-antagonist; and (3) animals receiving GnRH-antagonist as in group 1 plus 20 mg T-laden microspheres/testis. Treatment periods were 45 and 90 days. Serum T, testicular interstitial fluid T, testis weights, epididymal weights, daily sperm production (sperm x 10(6)/g/d), cauda sperm motility, and fertility were assessed in all animals. Gonadotropin-releasing hormone antagonist treatment reduced serum and testicular interstitial fluid to below detectable levels at day 45 and to similar levels at day 90. Supplementation with T-laden microspheres maintained testicular interstitial fluid T at concentrations not different from controls without elevation of serum T concentrations. All other values, including fertility were suppressed by GnRH-antagonist treatment and maintained by supplementation with T-laden microspheres.
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PMID:On the maintenance of male fertility in the absence of native testosterone secretion: site-directed hormonal therapy in the rat. 219 18

A sustained-release formulation of a potent gonadotropin-releasing hormone (GnRH) agonist, Zoladex (D-Ser(But),6 Aza Gly10-GnRH; ICI 118,630; goserelin), was administered subcutaneously (3.6 mg/depot) to male rats once every 28 days for 2-24 wk to determine the extent to which pituitary-testis function could be suppressed and whether suppression was maintained throughout the period of treatment. Administration of Zoladex resulted in sustained decreases in weight of the testis, epididymis, seminal vesicles and prostate gland. The decreases were apparent within 2 wk of initiating treatment. Patchy degeneration of the seminiferous tubules and atrophy of the Leydig cells were observed, but did not progress beyond the degree observed after 1 month of treatment. Serum and testis testosterone were markedly depressed after 2 wk of treatment, as was testis [125I]hCG binding. Serum gonadotropins were also reduced by treatment. Serum androgen binding protein (ABP) was elevated, testis ABP content remained unchanged, and epididymal ABP content was reduced. The changes are consistent with the hypothesis that this compound affects both the anterior pituitary gland and the testis. These findings indicate that depot delivery systems are a convenient way to administer GnRH analogs for sustained treatment schedules.
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PMID:Prolonged suppression of rat testis function by a depot formulation of Zoladex, a GnRH agonist. 253 93

Tissue sections from testes and epididymides obtained from 17 young beef bulls with scrotal circumference (SC) between 27 and 40.5 cm were studied to determine whether small testes were a manifestation of lesions or a result of less, but otherwise normal, seminiferous epithelium. The SC correlated negatively with the estimates of germinal epithelial loss and positively with seminiferous epithelial area. Four bulls with SC less than 30 cm had severe lesions in their testes. Hypoplastic tubules were characterized by Sertoli's cells only with no evidence of germinal cells. Loss of germinal cells, leaving vacuolated epithelium and atrophy, were observed in degenerated tubules. Hyperplasia of Leydig's cells was observed in the vicinity of Sertoli's cell-only tubules, resulting either from degeneration or hypoplasia, and atrophy of Leydig's cells was associated with tubules devoid of Sertoli's cells. These findings indicated that Sertoli's cells may produce a factor(s) required for maintenance and regulation of Leydig's cell function. Epididymal epithelium, especially in the head, had regressed in bulls with hypoplastic and degenerative changes in their testes. Decreased sperm concentration and motility and an increased frequency of morphologic defects were observed in the 4 bulls with testicular lesions and regressed epididymal epithelium. Blood plasma profiles of cortisol, follicle-stimulating hormone, luteinizing hormone, and testosterone were determined in the 4 bulls with SC less than 30 cm and 10 of the 13 bulls with SC greater than 30 cm. There were no statistically significant (P greater than 0.1) differences in the responses to exogenous gonadotropin-releasing hormone or base-line patterns of blood plasma follicle-stimulating hormone and luteinizing hormone between the 2 groups. However, in the bulls with SC less than 30 cm, the mean concentration of testosterone was lower, whether spontaneous (P less than 0.05) or exogenous gonadotropin-releasing hormone induced (P less than 0.1). The fact that these bulls were not deficient in gonadotropins indicated that Leydig's cell function was impaired by local factors, either the factors that caused the tubular damage or those consequent to the tubular damage.
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PMID:Pathophysiology of small testes in beef bulls: relationship between scrotal circumference, histopathologic features of testes and epididymides, seminal characteristics, and endocrine profiles. 309 13

m-Dinitrobenzene (m-DNB)-induced testicular atrophy has been attributed to a direct effect upon the germinal epithelium. However, such degenerative changes in the germinal epithelium should induce shifts in the testicular hormonal milieu, which would in turn alter the hypothalamic-pituitary gonadal axis in general. This study evaluated the endocrine status of male rats (killed 3 hr, 24 hr, 1 week, and 2 weeks) following a single oral dose of m-DNB (32 mg m-DNB/kg). Serum and pituitary leuteinizing hormone, follicle-stimulating hormone (FSH), and protactin and hypothalamic gonadotropin-releasing hormone (GnRH) concentrations were determined. Testosterone and androgen-binding protein concentrations in serum, interstitial fluid, seminiferous tubule fluid, and caput epididymis were also determined. In vitro basal and hCG-stimulated testosterone release was determined in the decapsulated testis. Results of the present study indicate that pituitary hormone concentrations and hypothalamic GnRH were unaffected after a single oral dose of m-DNB. Serum FSH was elevated at 2 weeks. There was a transient decrease in serum testosterone at 24 hr, which returned to control values at 1 and 2 weeks. Interstitial fluid, seminiferous tubule fluid, and caput epididymal testosterone concentrations were increased at 1 and 2 weeks. Basal testosterone release in vitro was increased at 2 weeks, while hCG-stimulated testosterone release was increased at 1 and 2 weeks. Androgen-binding protein concentrations in serum and interstitial fluid were increased at 1 and 2 weeks. Androgen-binding protein was increased at 24 hr and 1 week in seminiferous tubule fluid, but returned to control concentrations by 2 weeks. However, the total tubular content of androgen-binding protein was dramatically decreased at 2 weeks. Androgen-binding protein in the caput epididymis was unaltered following m-DNB treatment. These data demonstrate that m-DNB exerts a direct effect on the testes and not through alterations in hypothalamic and pituitary control of gonadal function.
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PMID:Changes in testicular and serum hormone concentrations in the male rat following treatment with m-dinitrobenzene. 313 88

Two courses of LHRH nasal spray (400 micrograms three times a day for 28 days), partly administered in a double-blind placebo-controlled study, resulted in the descent of 48 of 281 testes (18%) in 237 prepuberal boys. Logistic regression analysis confirmed the clinical observation that pretreatment testicular position was the major factor influencing treatment results: the lower the pretreatment testicular position, the better the result. Of the unsuccessfully treated boys, 170 with 196 undescended testes subsequently underwent orchiopexy revealing anatomic anomalies that accounted for failure of hormonal treatment in 80% of the cases. Most frequent finding amounted to an underdeveloped processus vaginalis, extending no further than the level of the pubic bone, often associated with major epididymal deformities and a lack of obliteration of the processus vaginalis (107 of 196 operations). Obstruction of the scrotal entrance due to abnormal Scarpa's fascia or abnormal gubernacular remnant was found in 35 and testicular absence in 15 cases. LHRH nasal spray might be effective when the testis can be manipulated to at least the scrotal entrance before treatment, but in view of our surgical findings, LHRH nasal spray will not replace orchiopexy.
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PMID:Why luteinizing-hormone-releasing-hormone nasal spray will not replace orchiopexy in the treatment of boys with undescended testes. 332 26

Adult male rats were treated daily for up to 8 weeks with histrelin, [(ImBzl)-D-His6, Pro9-NEt]LHRH, to study the antifertility effects of this LHRH agonist. Although serum testosterone concentrations and testicular sperm numbers were significantly decreased by weeks 2 and 4 respectively, a reduction in fertility, as judged by the mean number of fetuses per mated female, was not observed until the sixth week of treatment. Furthermore, the number of spermatozoa in the cauda epididymidis of treated rats did not decrease below initial control levels at any time during the study and full fertility returned within 4 weeks after histrelin treatment was stopped. Thus, the lack of correlation between fertility and testicular and epididymal sperm numbers suggests that the antifertility effects of LHRH agonists are not due solely to reduced sperm numbers, but also result from androgen deficiency.
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PMID:Lack of correlation between fertility and sperm numbers in male rats treated with histrelin, a potent LHRH agonist. 352 15

A highly potent agonist of LHRH, [6-D-(2-naphthyl)-alanine]-LHRH, was administered chronically for 12 weeks to adult male rats by repetitive implantation of pellets, and its effects upon mating, fertility, and reproductive organ weights have been evaluated. Although significant declines in testicular (P less than 0.001) and epididymidal (P less than 0.001) weights were achieved, no effects on seminal vesicles, prostate, or pituitary weights were observed. After 12 weeks of continuous treatment, three of six agonist-treated rats were still successfully impregnating females. The decline in successful impregnation appeared to be related to the observed reduction in testicular spermatogenesis and in numbers of epididymal spermatozoa. The drug effects appeared reversible, as all six of the agonist-treated rats were fertile by the fifth week after cessation of treatment. Plasma levels of testosterone were markedly elevated immediately after implantation of each pellet and consistently, but not significantly, lowered during the inter-implantation periods. These observations, and the lack of effect on accessory organ weights, are consistent with the maintenance of libido in these treated rats. This is the second demonstration of a selective inhibition of spermatogenesis in the absence of a marked decline in gonadal steroidogenesis with this agent. As in the first demonstration using twice weekly injections, the degree of inhibition of spermatogenesis was insufficient to abolish fertility in the treated male rats.
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PMID:Inability of continuous long-term administration of D-Nal(2)6-LHRH to abolish fertility in male rats. 622 58

Experiments were carried out in rats to characterize the development of the testicular and epididymal lesions and any associated effects on reproductive hormones. Adult F-344 rats were exposed to 3500 ppm methyl chloride (MeCl) 6 hr/day for 5 days, not exposed for 3 days, and exposed again for 4 days. The first consistent testicular lesion was a delay in spermiation which appeared on Day 9. Subsequently, germinal epithelial vacuolation and cellular exfoliation became widespread as exposure continued. All animals killed after 19 days also displayed bilateral epididymal granulomas in regions 5 or 6 of the cauda epididymis. The nature and distribution of inflammatory cells indicated that the primary neutrophilic response may be against the tubular epithelium and not extravasated sperm. After 5 days of exposure, circulating testosterone was below 6 ng/ml (control: 120 +/- 31 ng/ml). Both MeCl exposed and control animals responded similarly to challenge with hCG and LHRH ethylamide, suggesting that Leydig cell and gonadotrope function was unaffected. It is proposed that MeCl acts centrally to lower circulating testosterone. Nonprotein sulfhydryls were depleted in liver, testis, and epididymis after MeCl exposure, but not in whole blood. This finding indicates that sulfhydryl depletion is not due to direct alkylation, but is enzymatically mediated. Sulfhydryl depletion did not correlate with lesion development. It was concluded that the initial testicular effects of MeCl are directed at either the late stage spermatids or the Sertoli cells with a resultant delay in spermiation.
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PMID:Studies of lesions induced in the testis and epididymis of F-344 rats by inhaled methyl chloride. 638 32


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