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

The placement of epididymal obstruction at vasectomy was investigated to see if such placement affects the biological rejuvenation of males. Whether placing the obstruction proximal to the epididymis (Steinach II) instead of beyond it (Steinach I) would make any difference in dogs and men was investigated. Steinach II was studied in 15 dogs and 5 men. Occlusion was performed at the level of the vasa efferentia, avoiding any vascular trauma. Radiological visualization confirmed a perfect block. There were no untoward reactions, such as orchitis or hydrocele. In dogs, widespread degeneration in the seminiferous tubules was evident; total Leydig cell volume showed an increase from .7-1 ml/testis. These changes were not significantly different from conventional vasectomy. In men, there were considerable preexisting senile changes; total Leydig cell volume was already as high as 2.8 ml/testis. Hence, any possible effect of the Steinach II procedure was obscured by these preexisting changes.
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PMID:A second look at Steinach's second procedure: testiculoepididymal occlusion in man and dog. 44 25

Treatment of immature, hypophysectomized male rats with 50 micrograms ovine FSH (NIH-FSH-S12) twice a day for 5 days stimulated the maximum quantity of 17 beta-hydroxyandrogen produced by isolated Leydig cells in response to hCG. Pretreatment of the FSH preparation with an LH antiserum in one study markedly reduced and in another study completely abolished this stimulatory effect of FSH, but only slightly impaired the capacity of the hormone to stimulate the Sertoli cell in vivo (epididymal androgen-binding protein). Administration of another highly potent FSH preparation (LER-1881) had no discernible effects on the dose-response characteristics of the Leydig cells but was superior to the NIH-FSH-S12 in its capacity for stimulating the Sertoli cell. When all hormone preparations were tested for their ability to stimulate steroid secretion from normal Leydig cells in vitro, a close correlation was obtained between their Leydig cell-stimulating activity (a measure of LH contamination) and their capacity to alter Leydig cell responsiveness after in-vivo treatment. FSH treatment had no effects on specific LH binding per 10(6) Leydig cells. It is concluded that the stimulatory influence of FSH on rat Leydig cells may to some extent be a result of the LH contaminating the hormone preparation.
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PMID:LH contamination may explain FSH effects on rat Leydig cells. 57 30

The effects of local heating on testicular and epididymal vascular resistance in sodium pentobarbitone anesthetized rats was measured with a microsphere technique. When exposing the left scrotum to 33 and 37 degrees C for 30 min, no significant effects on blood flows were observed in comparison to those of the right side. Exposure to 41 degrees C caused a significant (p less than 0.05) decrease in vascular resistance of both testes and epididymides. The response was more pronounced at 43 degrees C. The Leydig cell function, as judged from the testosterone concentrations in plasma and testicular tissue after LH stimulation, was significantly (p less than 0.01) depressed at 41 and 43 degrees C. It was concluded that the impaired Leydig cell function was unrelated to testicular blood flow.
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PMID:The influence of scrotal warming on testicular blood flow and endocrine function in the rat. 69 55

Seminiferous epithelium histology, Leydig cell density, and in vitro testosterone synthesis were quantitated in bilateral testicular biopsies from men with varying degrees of unilateral or bilateral varicoceles. Results were correlated with plasma levels of gonadotropins (follicle-stimulating hormone [FSH], luteinizing hormone [LH]) and testosterone (T), as well as with semen quality. In patients with bilateral varicoceles, spermatogenesis, Leydig cell density, plasma T levels, and in vitro T synthesis were significantly lower than in patients with unilateral varicoceles. Varicoceles appeared to affect maximally the latest stages of spermatogenesis. A negative correlation between FSH and LH levels and spermatogenesis was observed; however, a dissociation between the two gonadotropins occurred when spermatogenesis declined. Plasma T levels were within the normal range in all patients. The T:LH ratio was significantly correlated with spermatogenesis and sperm motility. Leydig cell density was abnormally low in oligospermic patients, and it was significantly correlated with in vitro T synthesis, spermatogenesis, sperm motility, and semen volume. Sperm count and motility were significantly correlated in this group of patients, suggesting a common pathophysiology for the effect of varicocele on spermatogenesis and sperm motility. This common pathophysiology appears to be disturbed Leydig cell function resulting in decreased testicular androgen production, in turn causing inadequate spermatogenesis and epididymal function.
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PMID:A possible mechanism for the detrimental effect of varicocele on testicular function in man. 72 Jun 47

Danazol administration caused lesions in the seminiferous tubules of gerbils and mice. The seminiferous epithelium became systematically depleted of spermatogonia, spermatocytes, spermatids, and finally spermatozoa. Danazol administration did not cause damage to the epididymal cells but was followed by a significant increase (p smaller than 0.01) in the diameter of the Leydig cell nuclei. The growth of androgen-dependent organs was reversibly suppressed after treatment. Resumption of normal gonadal function in the mouse occurred 32 days after discontinuation of medication. Danazol brought about transient changes resembling those of bilateral gonadectomy in the anterior lobe of the hypophysis. Inhibition of endogenous gonadotropins occurred, reflected in the increased basophilic cell percentage.
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PMID:Effects of danazol on the pituitary-gonadal axis in male gerbils and mice. 110 42

A preliminary study of the effects of alpha-chlorohydrin on the reproductive tract of male dogs is presented. 10 animals were injected with 8 mg/kg/day of the drug for 30 days. The seminiferous tubules showed considerable degeneration and shrinkage. A gradual loss of type A spermatogonia, spermatocytes, spermatids, and spermatozoa was observed in the testes. The volume of Leydig cell cytoplasm increased, showing a granular appearance, and the nuclei were enlarged. Epididymides weights were significantly lower than those of controls (p less than .02). The epididymal lumen contained no spermatozoa and there was no evidence of obstruction. The synthesis of RNA and sialic acid was inhibited in the testis, caput epididymis, corpus epididymis, and cauda epididymis. Alpha-chlorohydrin significantly increased the total amount of cholesterol per gram/testis (p less than .02). Results indicate that alpha-chlorohydrin is antiandrogenic in nature and acts directly on the testis and epididymal biochemistry.
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PMID:Effects of alpha-chlorohydrin on the testes and epididymides of dog: a preliminary study. 115 64

It was recently demonstrated that the Leydig cell toxicant ethane dimethanesulphonate (EDS) produces multiple effects on the epididymis after a single in vivo exposure. To determine whether any of the perturbations were mediated by a direct action of the compound, we used a novel system for the coculture of epididymal epithelial cells and sperm from the caput epididymidis. This system maintains the morphologic integrity and cell polarity of the epididymal epithelial cells before and during coculture, and the sperm recovered after coculture have intact plasma and acrosomal membranes. In addition, several functions required for epididymal sperm maturation are expressed, including the secretion of protein by the epididymal epithelium, the association of secreted protein with the plasma membrane of cocultured sperm, and the acquisition of progressive motility by cocultured sperm. In vitro exposure of epididymal epithelial cells and sperm to EDS results in a significant decline in protein secretion by the epithelial cells during coculture, and in particular, a dose-dependent decline in a 36- to 38-kd protein (PI 4.0 to 4.5) and a 34- to 36-kd protein (PI 4.5 to 5.0). Moreover, these and other proteins are not recovered from the sperm membrane of cocultured sperm after EDS treatment. Finally, EDS results in a dose-dependent decline in the percentage of both motile and progressively motile sperm recovered after coculture compared with that of sperm from untreated cocultures. These effects on sperm motility were not observed when sperm were pretreated with EDS and subsequently cocultured with untreated epithelial cells. We conclude that EDS alters epididymal sperm maturation by acting directly on the epididymal epithelium to mediate changes in sperm membrane protein, and that this may subsequently alter the development of the progressive motility of sperm.
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PMID:Direct effects of ethane dimethanesulphonate on epididymal function in adult rats. An in vitro demonstration. 133 Oct 10

To study the effect of vitamin D deficiency on testicular function, 30-day-old male rats were put on a vitamin-D-deficient diet. At 120 days of age, the testicular function of these animals was compared with that of rats of the same age group fed, ad libitum, a diet containing vitamin D and rats fed on a restricted amount of diet with vitamin D. In vitamin-D-deficient rats, there was a significant reduction in the total body weight, testicular and epididymal sperm count and testicular glutamyl transpeptidase activity (an index of Sertoli cell function) as compared to control group rats, but there was no difference in the testicular lactate dehydrogenase activity (an index of germ cell function). Histological examination of the testis in vitamin-D-deficient rats revealed a significant reduction in the Leydig cell count along with degenerative changes in the germinal epithelium. Histological examination of the tibia revealed excess of osteoid in vitamin-D-deficient rats only. On the other hand, in undernourished rats given a normal amount of vitamin D, the only significant change was a reduction in total body weight. These results suggest that vitamin D deficiency retards spermatogenesis by interfering with the function of Sertoli and Leydig cells.
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PMID:Effect of vitamin D deficiency on testicular function in the rat. 147 57

Germ cells and Sertoli and Leydig cell functions were studied from 7 to 180 days after an acute exposure of 2-month-old rat testes to 9 Gy of gamma rays. Body weight, testis and epididymal weights were recorded. Sertoli cell parameters (androgen-binding protein, ABP, in caput epididymis and plasma follicle stimulating hormone, FSH) and Leydig cell parameters (plasma luteinizing hormone, LH, testosterone and prostate and seminal vesicle weights) were determined together with the number of germ cells and Sertoli cells. Irradiation did not affect body weight but significantly reduced testicular and epididymal weights from day 7 and day 15 post-irradiation respectively. The cells killed by irradiation were mainly spermatogonia and preleptotene spermatocytes engaged in replicating their DNA at the time of exposure, but all spermatocytes seemed damaged as they gave abnormal descendent cells. By day 34, only elongated spermatids remained in a few tubules and thereafter very little regeneration of the seminiferous epithelium occurred, except for one rat which showed a better regeneration. Levels of ABP decreased by day 15 when the germ cell depletion had reached the pachytene spermatocytes, whereas FSH and LH levels rose when the number of elongated spermatids decreased. Levels of testosterone and the weight of the seminal vesicles did not change; occasionally, the prostate weight was slightly reduced. These results support our hypothesis that pachytene spermatocytes and elongated spermatids are involved in influencing some aspects of Sertoli cell function in the adult rat.
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PMID:Effect of an acute exposure of rat testes to gamma rays on germ cells and on Sertoli and Leydig cell functions. 177 54

Adenomatoid tumors are regarded as uncommon neoplasms of the paratesticular tissues, probably of mesothelial origin. The majority of cases reported have involved the epididymis. We report our experience with 8 cases of testicular tumors and 11 of epididymal adenomatoid tumors during a 13-year period, and review the relevant literature. The incidence of adenomatoid tumors relative to all tumors in the testis was 6.9% (8 of 116), exceeding that of Leydig cell tumors, which were previously believed to be the most common benign testicular neoplasms. The adenomatoid tumors included 38% epididymal tumors (11 of 29). The clinical course of the tumors was benign, without recurrences. Local excision is regarded as the treatment of choice for epididymal and testicular adenomatoid tumors.
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PMID:Intrascrotal adenomatoid tumors. 205 7


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