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

Important advances have been made recently in our knowledge of hypothalamic-pituitary-testicular functions. Current understanding of the hypothalamic control of pituitary gonadotrophin secretion and the mechanisms of testicular feedback is beginning to yield benefits in the clinical management of certain reproductive disorders. But much remains to be learned about the neuroendocrine control of hypothalamic GnRH secretion--an area which encompasses the mechanisms regulating the onset of puberty. Spermatogenesis is a highly complex process involving subtle interactions between endocrine, paracrine and autocrine regulators acting on different cell populations within and without the testis. Until basic research can advance the very limited knowledge in this area, we cannot expect to improve the currently unsatisfactory management of infertile men. It is not surprising that only limited information can accrue from conventional semen analysis and measurement of systemic hormones. Nor is it unexpected that empirical or seemingly rational treatments for male infertility are of dubious benefit. In future, assessment of the infertile man should be improved by studying sperm functional capacities and testicular synthesis and metabolism of gonadal steroids and by the definition of representative markers of Sertoli cell and epididymal functions. Reversible male contraception is another objective that remains beyond our reach at present. Hormonal disruption of spermatogenesis is often incomplete and invariably suppresses Leydig cell function, so that androgen replacement for sustaining sexual function is mandatory. Alternative approaches to male contraception aimed at the epididymis and sperm-egg interaction seem more promising avenues for future exploration.
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PMID:Male hypogonadism--current concepts and trends. 393 78

In inbred CDF (Fischer 344) male rats autopsied at the age of 18-24 months, testicular tumors were present in 24 of 36 control animals but in none of 28 males rendered hyperprolactinemic by transplantation of anterior pituitaries from adult females under the renal capsules. In another experiment, microscopically detectable Leydig cell adenomas were present in each of 11 control animals at the age of 14.5 months but in none of 11 males in which hyperprolactinemia was induced by treatment with diethylstilbestrol. Development of testicular tumors had initially little effect on basal and hCG-stimulated plasma testosterone and androstenedione levels but eventually led to atrophy of the seminal vesicles. Incubated tumor tissue produced large quantities of progesterone and responded to hCG in vitro by an increase in progesterone but not testosterone secretion. Daily sperm production and epididymal sperm reserves were significantly reduced already during early stages of Leydig cell tumor development. We propose that hyperprolactin prevents development of Leydig cell tumors by suppression of plasma LH levels and suggest that age-related reductions in gametogenic and steroidogenic functions of the testes in Fischer rats are due to development of Leydig cell tumors rather than to aging per se.
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PMID:Hyperprolactinemia inhibits development of Leydig cell tumors in aging Fischer rats. 409 19

The effects of subcutaneous injections of prostaglandins F2 alpha and E1 (PGF2 alpha and E1) on the histophysiology of male reproductive organs of mature albino rats and their fertility rate were studied. Although most of the androgensensitive biochemical parameters were reduced by PG treatment, the level of cholesterol and activities of 3 beta and 17 beta hydroxy steroid dehydrogenases were not significantly altered in the testis. These results indicate a probable decline in target organ response to androgen and/or in conversion of testosterone to its metabolites. The reduction in fertility rate of prostaglandin-treated male rats has been correlated with the altered morphology of the epididymal spermatozoa as well as with their reduced density and motility. The weights of testis and epididymis were significantly reduced but those of seminal vesicle (SV) and ventral prostate (VP) were increased by PG treatment. The height of the germinal/secretory epithelium, the tubular diameter of testis, and the epididymis were decreased, but Leydig cell diameter was not affected. The reduced fructose in SV and the corresponding increase in its weight suggest that there is hypertrophy but no hyperplasia. On the other hand, in VP there probably occur both hypertrophy and hyperplasia. It is evident from the results that PGF2 alpha and E1 exert a definite growth promoting effect particularly in SV and VP together with the antiandrogenic and partial antifertility effects.
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PMID:Effects of prostaglandins on histophysiology of male reproductive organs and fertility in rats. 611 48

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

This study was designed to determine the effects of a short episode of testicular heating (43 degrees C for 15 min) on spermatogenesis and Sertoli and Leydig cell function. Rats killed at intervals up to 156 days after heating were assessed by histological examination, and by measurement of serum FSH and LH, and by tests of Sertoli cell function consisting of fluid production, androgen binding protein (ABP) content of the ligated and unligated tests, together with the binding of [125I]FSH. Leydig cell function was assessed by in vitro testosterone production, serum testosterone levels and [125I]hCG binding to testes homogenates. Testis weight declined 7 days after heating to 70% of control and remained lower until 82 days, whereas epididymal weight did not decrease significantly until 26 days and also recovered by 82 days. Fluid production was significantly lower in heated testes at 26 days and returned to normal at 56 days. ABP production measured as the difference between the ABP content of ligated and unligated testes was significantly reduced at 14 and 26 days, but subsequently recovered. Serum FSH levels were significantly elevated from 14-26 days in the heat treated group and the binding of [125I]FSH was reduced at 26 days post-heating. Basal and stimulated in vitro T production was significantly increased in the heat-treated testes at 14 days and subsequently returned to normal whilst [125I]hCG binding was significantly lower in the heat-treated testes from 7-26 days. Serum T and LH did not alter significantly during the study. Primary spermatocytes and young spermatids were the most heat sensitive germ cell type and a reduction in spermatogenesis was noted from 7 to 26 days, although recovery appeared complete by 56 days and thereafter. These results demonstrate that the transient spermatogenic disruption induced by heating is accompanied by significant alterations in Sertoli and Leydig cell function which are identical to those produced in other models of spermatogenic dysfunction. The results suggest that the duration of these changes appears to correlate closely with alterations occurring in the germ cell compartment.
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PMID:Changes in testicular function induced by short-term exposure of the rat testis to heat: further evidence for interaction of germ cells, Sertoli cells and Leydig cells. 643 36

The present investigations were carried out to show the histological and ultrastructural alterations in rat testes 10 weeks after gossypol acetic acid treatment (dose: 30 mg gossypol acetic acid/kg/day). the morphological findings in the interstitial compartment were compared with the data from studies carried out to investigate the testosterone biosynthesis in gossypol acetic acid treated rats. No morphological changes in the epididymal and vasal epithelia were found; however, the germinal epithelial cells showed vacuolisation, pycnosis, disconnections of junctions, cytolysis and exfoliation of germ cells from the epithelium. The Sertoli cells were affected, too. Gossypol acetic acid seemed to stimulate the physiological activity pathologically; cellular organelles as mitochondria, endoplasmic reticulum, lysosomal vacuoles, pigment granules and nuclei were either enlarged in size and number or malformed in shape. The cellular contact was often restricted to spots or completely disconnected. If gossypol acetic acid was administered for a longer period of time some Sertoli cells were found to be unable to withstand the toxic stimulus, and the cells became necrotic too. In contrast to the toxic process in the germinal and Sertoli cells the Leydig cell compartment did not show any changes in fine structure, and therefore testosterone biosynthesis is presumed to be intact.
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PMID:Ultrastructural analysis of rat testes after gossypol acetic acid (GAA) treatment. 686 21

Recent developments in the following areas of andrology are highlighted: varicocele; biochemical markers of epididymal function; genitourinary tract infection; evaluation of sperm motility; capacity for sperm fertilization; and the immunologic consequences of vasectomy. Discussion of the varicocele effect focuses on detection of thesubclinical varicocele, spermatic venography, Leydig cell functon, experimental models, and percutaneous venous treatment modalities. The size of the varicocele bears no relationship to its subsequent effects on spermatogenesis. Consequently, the "subclinical" varicocele, which is not palpable, becomes an important entity in the infertile patient. Use of a Doppler ultrasonic stethoscope for the detection of the nonpalpable varicocele and use of scrotal thermography have been reported although caution is advised with these techniques. The stress pattern is a nonspecific response of the germinal epithelium to a stimulus or the lack of a stimulus. Genitourinary infection or endocrinopathy can also cause an increased number of ejaculated immature sperm. Spermatic vein ligation is not justified in an infertile patient with a seminal stress pattern but without clinial evidence of a varicocele. Varicocelectomy also is unjustified in a patient with a palpable asymptomatic varicocele in the absence of a stress pattern. Venography in patients with varicocele should be reserved for individuals in whom persistence of a palpable or subclinical varicocele and abnormal semen parameters are observed following spermatic vein legation. It is also a research tool and can prove helpful in providing more information about testicular venous drainage. It may provide a vehicle for percutaneous treatment of the varicocele. Recent attention has been directed to a possible correlation between the presence of varicocele, Leydig cell function, and testosterone synthesis. The seminal stress pattern has been successfully produced in monkeys by a 90% constriction of the left renal vein between the vena cava and spermatic vein. The results indicated a bilateral testicular effect based on testicular biopsies. The conventional treatment for varicoceles is surgery. Recently, there have been reports of percutaneous, fluoroscopic treatment of these lesions. Originally considered to be a passive conduit for sperm transport, it is now evident that the epididymis is actively involved in the maturation of spermatozoa. The applicability of epididymal markers will be based primarily on the relative ease of determination in a clinical laboratory. Several newer methods for determining sperm motility -- turbidimetric techniques, laser light scattering techniques, and photographic tracking of sperm movement -- have been reported in an effort to increase objectivity, provide accurate records of sperm motilit, and study patterns of sperm movement and the effects of various exogenous agents. Vasectomy results in sperm antibody production. The presence of circulating sperm antibodies after vasectomy raises the possibility of systemic effects.
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PMID:Recent advances in male infertility research. 701 Jul 47

The male ACI rat has a congenital Wolffian duct defect manifested by unilateral agenesis of the kidney, ureter, seminal vesicle, ductus deferens, and most of the epididymis. In the adult the testis on the affected side is markedly smaller than the contralateral testis and spermatogenesis is absent. In addition, in vitro perfusion of the affected testis revealed significantly less testosterone secretion than did the contralateral testis. Moreover, electron microscopy revealed that the smooth endoplasmic reticulum of the Leydig cell was significantly decreased. Thus, the affected testes clearly showed deranged spermatogenesis and Leydig cell structure and function. The ACI rat model may provide insight into the potential effects of congenital epididymal abnormalities on the testis of the human.
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PMID:Testicular atrophy associated with agenesis of the epididymis in the ACI rat. 705 91

Chronic administration of solasodine (20 mg/kg alt. day for 30 days) caused testicular lesions resulting in a severe impairment of spermatogenic elements. The epididymides were devoid of spermatozoa. Total protein, sialic acid and glycogen contents of the testis and epididymis were reduced significantly whereas the testicular cholesterol was elevated. Acid Phosphatase enzyme activity of the testes was low after solasodine treatment. Serum enzymes (SGPT, alkaline phosphatase) serum protein, triglycerides, non esterified fatty acid levels were in normal range when compared with their own controls. Cholesterol and phospholipid levels were elevated after solasodine treatment to intact dogs. Reduced androgen production was reflected in low levels of sialic acid in the testes and epididymides and reduced Leydig cell nuclei. Castration alone brought about reduction in size of the epididymis. Castration followed by solasodine treatment caused epididymal degeneration. Simultaneous administration of TP to solasodine treated castrated dogs failed to stimulate the epididymal growth. Antispermatogenic/antiandrogenic activity of the compound solasodine is discussed. Solasodine administration in dogs definitely rendered the male infertile as evidenced by the absence of sperms in the cauda epididymis and ductus deferens.
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PMID:Antispermatogenic/antiandrogenic properties of solasodine (C27H43O2N) obtained from solanum xanthocarpum berries on the male genital tract of dog (Canis-familiaris). A histophysiological approach. 711 68

In the adult rat, ethane dimethanesulfonate (EDS) reduces testosterone (T) production by killing Leydig cells. Studies have also shown that acute EDS administration produces transient infertility and epididymal effects. Although these later effects were believed to be indirect results of the reduced Leydig cell T production, it was recently found that the epididymal effects were partially a direct result of in vivo EDS treatment. In contrast to the Leydig cells of the adult rat, immature Leydig cells are affected by EDS only at doses four- to sixfold higher than those that affect mature Leydig cells. In fact, the Leydig cells of the adult rat seem to be uniquely susceptible to the cytotoxic effects of EDS. Steroidogenesis in other organs, like the adrenal and ovary, are unaffected in vivo at doses that eliminate T production in males. In addition, studies have shown that doses of EDS that kill Leydig cells in vitro, isolated from the testes of adult rats, have no effect on similarly exposed hepatocytes. Hence, it was the objective of this study to describe the distribution and temporal fate of EDS in target (testes and epididymides) and nontarget tissues in immature and adult male rats and to determine if this information would explain either the age- or tissue-related susceptibility to EDS. We have concluded from this study that tissue distribution, integrated in vivo EDS dose, and differences in EDS metabolism are not the only factors contributing to the difference in sensitivity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Distribution of [14C]ethane dimethanesulfonate in immature and adult male rats following an acute exposure. 805 Jun 28


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