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A case of cyst of seminal vesicle associated with ipsilateral renal agenesis in a twenty-three-year-old man presenting primarily with rectal symptoms is reported. The usual symptoms had been urinary bladder irritation and pain on ejaculation. The embryologic development of this rare entity is discussed.
Tumours of the seminal vesicles were found in 11 of 182 male Han:Chin hamsters kept in a life-span study from weaning to their natural death. Histologically they were classified as adenocarcinoma (n = 10) and hemangiosarcoma (n = 1). The histopathological features of the neoplasms are described.
Calcification of the seminal vesicles and vasa deferentia is rare. Only the second idiopathic case recorded is presented herein. This case highlights the need to exclude serious, but treatable diseases associated with this condition, which are not generally considered on initial presentation.
A seminal vesicle cyst was found in a 30-year-old man with ipsilateral renal agenesis. His sister had embryologically analogous malformations--Gartner duct cyst, bicornuate uterus and renal agenesis. This seems to be the first reported familial occurrence of these combined malformations. The embryogenesis is reviewed and the diagnostic procedure and treatment are discussed.
A 72-year-old man with a seminal vesicle carcinoma is reported. The patient was treated by local excision of the tumour and radiotherapy. When the patient deteriorated and radiological and scintographic signs of skeletal metastases developed, hormone therapy (oestrogen) was initiated. Within a few weeks the patient was free from his severe pain. The radiological and scintographic signs of metastases had either diminished in size or disappeared after one year of oestrogen therapy. The patient is still alive and well 2 years after the diagnosis was established.
A basic 54-kDa protein (pI approximately 8.8) that cross-reacts with anti-caltrin antisera has been detected and isolated by gel filtration and cation exchange chromatography from seminal vesicle content of the rat. The soluble protein spontaneously precipitated in NaHCO3-buffered solution at pH 7.8, but it was kept soluble in imidazole buffer containing EDTA and dithiothreitol at pH 7.0. In addition to the main band of 54 kDa, two faint immunoreactive fractions with molecular weights around 45,000 and 14,000 were also revealed by Western blotting. The presence of the rat caltrin sequence within the primary structure of the 54-kDa molecule has been investigated by sequencing the peptides generated by trypsin digestion. The sequence of the first 46 amino acid residues of rat caltrin has been found in one of the fragments produced by enzymatic cleavage. However, the exact location of the caltrin sequence in the whole 54-kDa protein has not been determined. The purified 54-kDa protein did not inhibit Ca2+ uptake by epididymal spermatozoa. Results indicated that this molecule represents an inactive precursor of caltrin and is enzymatically processed in the lumen of the seminal vesicle to the small and active calcium transport inhibitor protein. The immunoreactive proteins with intermediate molecular weights (45,000 and 14,000) could represent partially degraded products of the precursor. The lack of inhibitory activity of the precursor may be related to the molecule's having a size and conformation that would make it unable to interact with caltrin receptors on the sperm surface.
One of the major proteins secreted from the rat seminal vesicle epithelium, namely SV-IV, was shown to act in vitro as acyl donor and acceptor substrate for transglutaminase from both guinea pig liver and rat anterior prostate secretory fluid. Electrophoretic and chromatographic experiments indicated that the enzyme catalyzed the formation of multiple modified forms of SV-IV. In the absence of small Mr amines, transglutaminase was able to produce at least six different molecular forms of the protein, half of which possessed an Mr higher than that of native SV-IV. These findings suggested that a variable number of intermolecular, and perhaps intramolecular, crosslinks were formed between one or both glutamine residues and one or more lysine residues occurring in the SV-IV polypeptide chain. In addition, at least three modified forms of the protein were produced by transglutaminase in the presence of high concentrations of spermidine, thus indicating the formation of different (gamma-glutamyl)polyamine derivatives of SV-IV. Rabbit uteroglobin and rat anterior prostate secretory protein(s) were also shown to be able to covalently bind spermidine in the presence of the enzyme. The possible biological significance of transglutaminase-mediated modifications of SV-IV, as well as of other proteins occurring in the mammal seminal fluid, are discussed.
OBJECTIVE: To determine the distribution and patterns of co-localization of nitric oxide synthase (NOS), neuropeptides and tyrosine hydroxylase (TH) in intrinsic nerves of the human post-natal vas deferens and seminal vesicle. MATERIALS AND METHODS: Double and triple immunolabelling methods were used in tissue from 10 male infants and children (age range 2 months to 3 years) obtained at post-mortem examinations carried out within 12 h of death. RESULTS: Most nerves supplying the muscle coat of either organ were TH-immunoreactive (-IR), most of which also contained neuropeptide Y (NPY) while a smaller proportion contained both NPY and NOS. Minor populations of the TH/NPY-IR intramuscular nerves contained calcitonin gene-related peptide (CGRP), galanin (GAL), met-enkephalin (m-ENK) or vasoactive intestinal polypeptide (VIP). Non-TH-IR intramuscular nerves were relatively infrequent and most contained NPY and either VIP or NOS. Presumptive secretomotor nerves formed subepithelial plexuses in both organs, most of which contained NPY co-localized with either VIP or NOS, with minor populations containing CGRP and/or GAL. TH- and substance P (SP) -IR nerves were not observed subepithelially. Perivascular nerve plexuses were mainly formed by TH-IR varicose nerves, most of which contained co-localized NPY and CGRP, with a smaller proportion containing NPY and NOS and minor populations containing VIP, m-ENK, SP or GAL. CONCLUSION: These results indicate that the autonomic control of the human vas deferens and seminal vesicle is provided by several immunohistochemically distinct nerve populations. Furthermore, NOS is present in a proportion of both the noradrenergic and non-noradrenergic nerves. Pharmacological studies are now required to elucidate the precise roles of nitric oxide and neuropeptides in the functional control of these organs.
The genomic structure of an androgen-stimulated mouse seminal vesicle autoantigen was determined. Analysis of the nucleotide sequence established 2135 bp of the 5'-flanking region, four exons of 123, 136, 112, 227 bp, three introns of 1555, 1931, 316 bp, and 185 bp of the 3'-flanking region of this gene. Ten DNA segments, five in the 5'-flanking region, two in the first intron, and three in the second intron were identified to have more than 50% homology with the consensus sequence of the androgen response element (ARE). Two sets of adjacent DNA segments, one including -213 to -199 bp and -124 to -110 bp in the 5'-flanking region and the other including 2532 to 2546 bp and 2582 to 2596 bp in the second intron, are noticeable for their high degree of homology with ARE.
A single maternal dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on gestation day (GD) 13 can greatly impair ventral prostate, dorsolateral prostate, anterior prostate, and seminal vesicle development in wild-type C57BL/6 mice. The developmental stages at which these organs are most sensitive to TCDD exposure have now been investigated. Pregnant mice were dosed orally with 5 micro g TCDD/kg or vehicle on GD 13, and their pups were fostered at birth to dams of the same treatment or cross-fostered to dams of the opposite treatment. Additional males had in utero and lactational TCDD exposure following maternal dosing on GD 16. Organ weights and secretory protein, cytokeratin 8, and cyclophilin mRNA expression were determined at 35 days of age. Effects of TCDD on ventral prostate development were due primarily to in utero exposure; the critical window was between GD 13 and birth. Dorsolateral prostate development was inhibited about equally by in utero or lactational exposure, and vulnerability did not begin until GD 16. Anterior prostate development was also affected by both in utero and lactational TCDD exposure, particularly the former. Vulnerability began before GD 16 and continued into postnatal life. Seminal vesicle development was essentially unaffected by in utero or lactational exposure alone but was significantly inhibited by combined exposure, regardless of whether dams were dosed on GD 13 or 16. In summary, the time during which each organ was most vulnerable to TCDD exposure varied from one organ to another. These findings provide insights into the developmental processes that TCDD inhibits in each organ, and demonstrate that TCDD inhibits ventral prostate development before this organ first appears, presumably via effects on the urogenital sinus. The observation that in utero TCDD exposure (alone) inhibited development of each prostate lobe is significant because previous studies have shown that little TCDD is transmitted to mice before birth.
1. Two basic proteins were purified from secretions of rat seminal vesicles by using Sephadex G-200 chromatography and polyacrylamide-gel electrophoresis under denaturing conditions. 2. It is not certain that these two proteins are distinct species and not subunits of a larger protein, but their properties are similar. Highly basic (pI = 9.7), they migrate to the cathode at high pH and their amino acid composition shows them to be rich in basic residues and serine. Threonine and hydrophobic residues are few. Both proteins are glycoproteins and have mol.wts. of 17000 and 18500. 3. Together these two proteins account for 25-30% of the protein synthesized by the vesicles, but they are absent from other tissues. 4. Changes in androgen status of the animal markedly affect these proteins. After castration, a progressive decrease in the basic proteins is observed and the synthesis of the two proteins as measured by [35S]methionine incorporation in vitro is is decreased. Testosterone administration in vivo rapidly restores their rates of synthesis. 5. These effects on specific protein synthesis are also observed for total cellular protein, and it is suggested that testosterone acts generally on the total protein-synthetic capacity of the cell and not specifically on individual proteins. Proliferative responses in the secretory epithelium may also be involved. 6. The extreme steroid specificity of the induction process suggests that the synthesis of these basic proteins is mediated by the androgen-receptor system. 7. The biological function of these proteins is not clear, but they do not appear to be involved in the formation of the copulatory plug.
Addition of arachidonic acid to ram seminal vesicle microsomes oxidizes 3,4-dihydroxy-3,4-dihydrobenzo[a]anthracene (BA-3,4-diol) to five more polar products. Four of the products are identified by chromatographic and spectroscopic analysis as tetrahydrotetraols, which are solvolysis products of dihydrodiolepoxides. The fifth product is a 10-methyl ether formed by methanolysis of the anti-diolepoxide. Quantitation of the individual products indicates that anti-diolepoxides predominate over syn-diolepoxides by approximately 2:1. Identical product profiles are detected from the reaction of BA-3,4-diol with hematin and 13-hydroperoxy-octadecadienoic acid in the presence of Tween 20. No other products are detected in either system, which indicates that peroxyl radicals oxidize BA-3,4-diol exclusively by epoxidation of the 1,2-double bond. The stereochemical and regiochemical differences between oxidation of BA-3,4-diol by peroxyl radicals and cytochrome P-450 are dramatic and suggest that BA-3,4-diol is uniquely suited as a probe to quantitate peroxyl radical-dependent epoxidation in vitro and in vivo.
The processing of secretory proteins in the guinea pig (GP) seminal vesicle epithelium (SVE) is altered by castration and restored by treatment of animals with androgens. To test the hypothesis that the changes in protein processing are due to changes in the activity of specific proteases, we examined the GPSVE for protease activities capable of cleaving a synthetic elastase substrate, succinyl-alanyl-alanyl-alanyl-p-nitroanilide (Suc(Ala)3pNA). We found that the GPSVE does contain a Suc(Ala)3pNA-cleaving activity that is sensitive to the serine protease inhibitor diisopropylfluorophosphate (DFP) and to the elastase inhibitor elastatinal. Furthermore, the amount of protease activity per milligram of SVE protein is reduced to about 50% of control levels by castration. The activity is completely restored within four days by treatment of castrated animals with androgens, but is not restored by treatment with estradiol, progesterone, or dexamethasone. Although the SVE enzyme did not yield a pattern of specific cleavage products when incubated with a secretory protein substrate in vitro, this enzyme activity was competitively inhibited by a peptide whose primary sequence included the cleavage site used by the processing machinery in vivo.
1. The guinea-pig seminal vesicle has been shown to be a very suitable test object for the study of mechanisms involving alpha-adrenoceptive receptors, because no beta-receptors were found in this preparation.2. Adrenaline, noradrenaline and phenylephrine were directly acting agonists, their ED50 values being 7.1 x 10(-6)M, 1.5 x 10(-5)M and 2.7 x 10(-5)M, respectively.3. Pretreatment with reserpine had no influence on the contractions caused by adrenaline, noradrenaline and phenylephrine but abolished or greatly reduced the contractions caused by dopamine. Cocaine enhanced the effects of adrenaline, noradrenaline and phenylephrine and reduced those of dopamine.4. Pronethalol (6.8 x 10(-5)M) reversed the alpha-receptor blockade by dibenamine, ergotamine and phentolamine of responses to adrenaline, noradrenaline and phenylephrine; it did not affect the blockade by dibenamine of responses to histamine.5. Reversal of the blockade by dibenamine was observed only when its concentration was such that it caused a parallel shift of the dose-effect curves of the agonists to the right; higher concentrations, which caused an unsurmountable depression of the maximal contraction, were not antagonized by pronethalol.6. It is assumed that the reversal is dependent on a direct action on alpha-receptors, "spare receptors" being probably involved.
The effects of suramin on the growth of seminal vesicles (SVs) of neonatal mice were investigated in vitro. SVs from 0-day-old male mice were cultured in serum-free chemically defined medium supplemented with 5 alpha-dihydrotestosterone (DHT, 10(-8) M) and insulin (10 micrograms/ml), alone and in combination. Prior to culture, SVs from 0-day-old mice had no epithelial branches. SVs cultured in medium with DHT formed numerous epithelial branches, while epithelial branching did not occur in SVs cultured without DHT. The addition of suramin (0.2 mM) to medium containing DHT inhibited the formation of epithelial branches almost completely. Removal of suramin from the medium on days 2, 4, and 6 of culture initiated the formation of epithelial branches. Suramin (0.2 mM) reversibly decreased 3H-thymidine-labeling indices (3H-LI) of both epithelium and mesenchyme of SVs cultured in medium with DHT plus insulin or DHT alone during 8 days of culture. Suramin also decreased 3H-LI of both epithelium and mesenchyme of SVs cultured in medium with insulin alone. The present study indicates that suramin reversibly inhibits not only androgen-dependent but also androgen-independent growth and ductal branching morphogenesis of neonatal mouse SVs.
At the apex of the epithelial principal cells of the seminal vesicle, there appears to be two types of mature secretory granules, i.e., large and small. Both types of secretory granules showed an eccentric electron-dense spherical body with one pole attached to the delimiting membrane. The remainder of the large granule surrounding the eccentric body showed a granulofilamentous texture, whereas that of the small granule was electron lucent. The formation of these two types of granules was traced back to the various elements of the Golgi stacks. In the case of the large granules, the earliest stage of segregation of the precursor of the eccentric dense body was observed in distensions of the cis-element. Within distensions of all subjacent saccules, the dense bodies continued to be present but progressively increased in size while remaining attached to the saccular membrane. Following separation from the trans-face of the stack, the large prosecretory granules continued to increase in size by fusing with each other. The very large prosecretory granules, as they migrated toward the cell apex to become mature secretory granules, reduced in size prior to exocytosis. The small granules formed exclusively on the trans-aspect of the Golgi stacks and did not appear to fuse with each other. Observations on the formation of the large prosecretory granules within the Golgi apparatus and of the eccentric body in particular, which may be taken as a marker of the saccular membrane, were suggestive of a cis-trans migration and renewal of Golgi saccules.
With the use of retrograde tracing techniques, selective spinal nerve transections, and immunohistochemistry to label noradrenergic and peptidergic pathways, this study has for the first time defined in detail the autonomic innervation to the rat seminal vesicles. The majority of this innervation originates from the bilateral major pelvic ganglia, whereas very few neurons are located in the accessory, inferior mesenteric, or paravertebral chain ganglia. Neuropeptide Y was the most abundant marker, followed by tyrosine hydroxylase (an enzyme involved in noradrenaline synthesis), and then vasoactive intestinal peptide. Sympathetic axons with tyrosine hydroxylase and neuropeptide Y supplied vascular and nonvascular smooth muscle whereas parasympathetic, cholinergic neuropeptide Y terminals were associated with the glandular epithelium. In contrast, vasoactive intestinal peptide was found only in cholinergic neurons, which may have either parasympathetic or sympathetic spinal connections. The latter were far more prevalent, demonstrating a substantial sympathetic cholinergic innervation to the seminal vesicles. Vasoactive intestinal peptide axons were associated with the glandular epithelia, as well as vascular and nonvascular smooth muscle. Axons associated with the secretory epithelia may regulate secretion or perhaps provide trophic support. Finally, acute damage to preganglionic sacral and lumbar nerves caused a transient increase in glandular weight.
Endogenous levels of the polyamines putrescine, spermidine, and spermine have been examined in the 10(6) m/s2 supernatant of different lobes of the rat prostate and in the seminal vesicles of castrates, androgen-stimulated castrates, and intact controls. Content of the polyamines varied between the lobes, with spermidine highest in intact animals. After castration, the content of polyamines fell significantly in all lobes but the coagulating gland (CG). Spermidine levels were highest, except in the lateral prostate (LP) and CG, where the content of putrescine was highest. In castrated animals treated with testosterone propionate for 72 h, the amount of the three polyamines examined increased dramatically in the ventral prostate (VP) and moderately in the CG and seminal vesicle (SV). Concerning individual polyamines, spermidine increased significantly in all lobes, while putrescine increased significantly only in the two saccular parts of rat prostate, i.e., CG and SV. Spermidine content decreased significantly in the DP. Major differences in the content of the three polyamines--putrescine, spermidine, and spermine--in the various tissues studied have been found. Moreover, distinct differences among intact, castrated, and testosterone-treated castrated animals have been revealed.