Male Sex Glands Research Articles

Biochemical characteristics and biological profile of prostate specific antigen (PSA)

Since its identification in seminai fluid in 1971, a tot more knowledge has been obtained about the biology and expression of prostate specific antigen (PSA). PSA is a glycoprotein consisting of 93% aminoacids and 7% carbohydrates with a molecular weight of about 30000 dalton. Functionally and structurally PSA is a kallikrein-like serine protease and its physiological role is the degradation of the major proteins of the seminal coagulum (semenogelin I and II, fibronectin) leading to semen liquefaction. The PSA gene is located on the 13q region of chromosome 19 and has a high degree of homology (more than 80%) with the gene of human glandular kallikrein (hGK1). PSA production and expression are preferentially but not exclusively associated with the normal, benign hyperplastic and cancerous tissues of the prostate. In fact, it has been demonstrated that PSA is also present in the accessory male sex glands of Cowper, Littre and Morgagni and other extra-prostatic neoplasms, such as salivary gland tumours and breast cancer. Many factors may influence PSA synthesis and production and among them the most important are androgen and growth factor stimulation. Advances have recently been made on the molecular isoforms of PSA. In the seminai fluid PSA seems partially bound to a serpine (protein C inhibitor), whilst in the serum PSA is predominantly associated to α-antichymotrypsin (ACT) and in low quantity to α2-macroglobulin (α2M). All these findings will have implications on clinical applications of PSA as a tumour marker for prostate cancer.

A 17‐kDa CD4‐binding glycoprotein present in human seminal plasma and in breast tumor cells

We previously isolated gp17, a human seminal plasma glycoprotein, which specifically interacts with the D1-D2 region of CD4, a T cell surface molecule involved in antigen recognition mediated by helper T cells also acting as a receptor for the human immunodeficiency virus. In this study we report that monoclonal antibodies (mAb) reacting with gp17 are able to inhibit the binding of gp17 to immobilized soluble CD4. An immunohistochemical analysis shows that gp17 is also expressed in mammary tumor cells upon hormone treatment and in biopsies from breast cancer patients. A structural characterization of gp17, including amino acid sequencing, indicates that the protein has an extensive structural similarity with a glycoprotein designated as seminal actin-binding protein (SABP), also secreted by male sexual glands. SABP is in turn identical to gross cystic disease fluid protein-15 (GCDFP-15) or prolactin-inducible protein (PIP), a factor known as a highly specific and sensitive marker of primary and metastatic apocrine breast cancer. To establish further the correspondence of gp17 and GCDFP-15/PIP/SABP, the latter was expressed in bacteria from a cloned cDNA and purified by affinity chromatography to either anti-gp17 mAb-Sepharose or CD4-Sepharose. The purified recombinant protein is shown to inhibit the binding of labeled, pure g17 to immobilized soluble CD4. The finding that breast cancer cells express a protein able to interact with the CD4 domains involved in the recognition of class II major histocompatibility antigens suggests a possible mechanism by which a tumor may affect the activity of tumor-infiltrated CD4+ T cells.

Immunohistochemical localization ofprostate-specific markers within the accessory male sex glands of Cowper, Littre, and morgagni

Objectives. The aim of the study was to explore possible production of prostate-specific markers by the embryologically and physiologically related accessory male sex glands, other than the prostate. Methods. The accessory male sex glands of Cowper, Littre, and Morgagni were studiedsystematically in 10 whole-mount autopsy and 5 surgical cystoprostatourethrectomy specimens. Immunohistochernistry was applied with the avidin-biotin-peroxidase method and commercially available monoclonal antibodies raised against prostate-specific antigen (PSA) and prostate-specific acid phosphatase (PSAP). Results. All specimens showed clear microscopic identification of these glands exceptfor Cowper's glands, which were not found in most of the surgical cystoprostatourethrectomy specimens but were found coincidentally in one. Localization of the prostate-specific markers PSA and PSAP was demonstrated for the first time in three Cowper's glands, but they were a consistent finding in Littre's and Morgagni's glands when immunohistochemical identification was performed in a systematic fashion. Conclusions. PSA and PSAP are mostly produced by prostatic tissue, but not exclusively.These findings may have an impact on the specificity and sensitivity of PSA serum levels after radical prostatectomy because they support the hypothesis of extraprostatic sources of PSA.

The Neglected Sex Gland

T ucked away under the bladder in a man's body is the walnut-size prostate gland that often labors away under a cloak of anonymity Many men don't know they have this male sex gland. Others don't know where the prostate is located or what it does. And when something goes wrong with the prostate, even doctors can't always tell whether the condition is a life-threatening cancer or a relatively harmless enlargement. For much of a man's life, the prostate gland produces some of the fluid, or semen, that carries sperm through the urethra during sexual climax. But after age 50, the prostate can begin causing trouble. For reasons not well understood, the prostate gland often gets larger as a man ages. Indeed, more than half of all men in their 60s suffer from an enlarged prostate, a condition called benign prostatic hyperplasia (BPH). If the gland gets too big, it can squeeze the urethra, the tube that also carries urine from the bladder. This pressure can cause a weakened or hesitant urine stream or an increased need to urinate, especially at night. While the symptoms of BPH can be annoying, a second, more serious threat involving the prostate gland plagues older men: cancer. Men with BPH are not at increased risk for prostate cancer; however, symptoms of prostate cancer and BPH are often identical. Even worse, doctors don't have a foolproof diagnostic test to distinguish between BPH and cancer of the prostate, a disease that will kill an estimated 34,000 men in the United States in 1992 alone. Until recently, doctors looking for prostate cancer had to rely on a test known as the digital rectal exam. After pulling on gloves, the physician inserts a finger into the rectum and probes for any hard lumps that may indicate the presence of cancer. While this time-honored test does reveal some malignancies, it misses a large number of prostate tumors. Furthermore, the rectal exam often turns up only advanced cancers those that have spread beyond the prostate wall and thus are more deadly Within the last few years, a protein known as prostate-specific antigen (PSA) has taken center stage in the fight against this potentially lethal cancer. For some time after PSA's discovery more than 20 years ago, the molecule attracted little attention. Then, during the 1980s, a slew of researchers began to take another look at PSA. The scientific community's renewed interest in accelerated about a year ago, when William J. Catalona of the Washington University School of Medicine in St. Louis and his colleagues published a pioneering report on and prostate cancer. By measuring the concentration of in the bloodstream, Catalona's team found they could detect more prostate cancers than they could by relying on the rectal exam alone. We found that was the most powerful test we had, Catalona says about the study, reported in the April 25, 1991 NEW ENGLAND JOURNAL OF MEDICINE. The findings fueled a virtual boom in blood tests ordered by doctors around the country More than a year later, most scientists would agree that, although a powerful predictor of prostate cancer, has shortcomings. Still, PSA may be better than anything we have, even though it's not perfect, Catalona says. His group and several other research teams are now searching for ways to refine PSA's ability to flag prostate cancer and distinguish it from a harmlessly enlarged prostate.

Protein C inhibitor in human body fluids. Seminal plasma is rich in inhibitor antigen deriving from cells throughout the male reproductive system.

An assay was developed for the measurement of human protein C inhibitor antigen (PCI) in blood plasma and other biological fluids. Both native PCI, modified inhibitor, and complexes of inhibitor with activated protein C or plasma kallikrein could be measured with the assay. Inhibitor antigen concentrations were found to be very high in seminal plasma (greater than 200 mg/liter), more than 40 times the concentration of PCI found in blood plasma. The inhibitor in seminal plasma was unable to form complexes with activated protein C. Gel filtration and immunoblotting findings indicated that the inhibitor in seminal plasma is present in a high molecular mass complex or cleaved to its modified form. As PCI antigen was absent from seminal plasma of patients with dysfunctional seminal vesicles, the seminal vesicle glands would appear to be the major source of seminal plasma PCI, a conclusion supported by immunohistochemical demonstration of the presence of PCI epitopes in the secretory epithelium of the seminal vesicles. Specific PCI immunoreactivity was also shown to be present in the testes, the epididymis glands, and the prostate, suggesting the inhibitor to have a complex or multiple function in the male reproductive system. Conclusive evidence of a local synthesis of PCI in the four male sex glands was provided by Northern blot analysis of RNA from these organs.

Frequency and Distribution of Uropathogenic Escherichia coli Adhesins: A Clinical Correlation over 2,000 Cases

In order to determine the pathogenic responsibility of Escherichia coli adhesins (ADHs) in urinary infections (UI), 2,000 different patients suffering different clinical urinary and male sexual gland infections were monitored. The ADHs were determined by agglutination techniques with human and guinea-pig red blood cells, Candida albicans and Saccharomyces cerevisiae cells and latex sensitized with GAL-GAL. In uncomplicated UIs, the possession of ADH is the main invasion mechanism for E. coli. The rate of E. coli ADH strains is very high (89%) in acute cases (727 of 818 cases: 310 of 362 cystitis; 104 of 113 recidivant cystitis; 120 of 126 pyelonephritis; 158 of 173 prostatitis, and 34 of 43 orchiepididymitis) and rare (10%) in asymptomatic or chronic cases (24 of 235 cases: 14 of 148 bacteriurias; 8 of 74 prostatitis, and 2 of 13 orchiepididymitis). A close relation is established between the presence of ADH and clinical symptoms. 90% (218 of 242) of acute cases with systemic symptoms are due to MR-type ADH strains, especially the P subtype. 71% (409 of 576) of acute cases with local symptoms are due to MS-type ADH strains. In complicated UIs the expression of ADH is not an essential condition for the invasion of the urinary apparatus. It has been strongly suggested that males are significantly more resistant to UI, both in the tract and parenchyma, than women. It can be deduced that the underlying disease is more liable to UI the lower the adherence level shown by isolated strains. Thus catheters, reflux and neurogenic bladder are, by far, more aggressive alterations than the prostatic adenoma, vesical tumor or lithiasis.

Pathways of activation and change of the endocrine function of testes elicited by effect of presence of the female

1. The presence of a receptive female elicits a maximal rise, governed by the synchronous augmentation of its biosynthesis in the male sex gland, in the level of T in the blood plasma and testes in male mice within 20–40 min. Blood T and its production by the testes become normalized by the 80th minute, whereas normalization of its content in the male sex gland takes place later. 2. The activating effect of the presence of a receptive female on the blood level of T is achieved with the involvement of luliberin receptors by the transadenohypophyseal pathway, since a luliberin antagonist completely blocks this effect.

Intersex mice composed of androgen insensitive Tfm and wild-type cells analysed by 3H dihydrotestosterone autoradiography.

The X-linked testicular feminization mutation (Tfm) in the mouse is characterized by an androgen receptor defect. Due to random X-chromosome inactivation, XTfm/X+ heterozygotes are mosaics with respect to Tfm. They are composed of androgen receptor deficient XTfm cells and normal X+ wild-type cells. If Tfm heterozygotes are converted to XX males by the sex reversal factor (Sxr) the mosaicism is expressed. Therefore in sex reversed Tfm heterozygotes (XTfm/X+-Sxr) intersexual sex organs develop. In five intersexes with small male accessory glands and hypospadia and one heavily feminized intersex with vagina and caudally dislocated deferent ducts the mosaic is visualized by 3H-DHT-autoradiography. In the epididymis differentiated wild-type cells show nuclear labeling, whereas undifferentiated Tfm cells are unlabeled. Unlabeled Tfm cells are also encountered in the vesicular glands of the heavily feminized animal, demonstrating that Tfm cells can participate in the formation of male sex glands. The urethral glands of the mosaic animals are composed of unlabeled Tfm lobules exhibiting the female phenotype of the glands, and of labeled wild-type lobules exhibiting the male phenotype. Formation of a vagina and deviation of the deferent ducts is correlated with lack of androgen binding sites in the connective tissue.

The reproductive cycle of male tomb bats, Taphozous hildegardeae (Chiroptera: Emballonuridae), in a seasonal environment of the African tropics

Two cave populations of Hildegarde's tomb bat had a reproductive cycle that corresponded closely to the rainfall‐induced seasonality of coastal Kenya (4s). Males had pronounced bimodal cycles of body weight due to the deposition of fat during periods of relative food abundance in both rainy seasons, and fat depletion during competitive mating and the dry seasons, when numbers of moths were lowest. The main period of sexual regeneration coincided with the increase in body weight experienced during the ‘long rains’ [April‐June) and led to mating. A secondary peak in the weights of male sexual glands, associated with the increase in body weight that occurred in the ‘short rains’ (October‐December), did not result in reproduction. It is suggested that this latter period of sexual activity was related to the maintenance of year‐round harems, and may represent the male response to a vestigial, bimodally polyoestrous, reproductive cycle.

Cysteine proteinase inhibitors in human and rat male sex glands.

The testis and prostate of men had two types of cysteine proteinase inhibitors of different isoelectric point (pI = 4.5 and 6.3) and molecular masses (90,000 and 12,000). The seminal vesicle contained not only these two inhibitors but also a basic inhibitor with a pI = 9.5 and Mr 11,000. In rats, the inhibitors in the testis and prostate consisted of two types with pI values of 4.3 and 4.8 and Mr 90,000 for both. In addition to these two inhibitors, the seminal vesicle contained large amounts of two basic inhibitors with pI values of 7.5 and 8.3 and Mr of 11,000 for both. We suggest that the basic cysteine proteinase inhibitor found in semen might be excreted from or be modified in the seminal vesicle.

Effect of prolactin, testosterone and estrogen on prolactin binding in the rat testis, prostate, seminal vesicle and liver

We have studied the hormonal control of prolactin (PRL) binding in the male rat sex glands and liver, subsequent to the recent demonstration and characterization of specific PRL binding sites in rat testis, prostate and seminal vesicle. Ovine PRL (200 μg/rat/day, 7 days) caused a time-dependent reduction in testicular binding of 125I-labelled PRL (measured 2 days after last injection) to 58% of control. Testosterone alone (1 mg/rat/day, 7 days) or PRL caused similar reductions in binding, while their coadministration further lowered PRL binding to 10% of control. The synergism of PRL and testosterone suggests that either these doses are submaximal, or that they are acting on different systems. Estradiol was administered as a single dose of 2 mg/rat and the PRL binding determined on day 10 and day 19 was reduced to 37% of control, as after testosterone. Addition of PRL whether from day 1 to day 7 or from day 11 to day 17 of estradiol injection had no effect, suggesting that the EB site of action is closer to the PRL receptor than that for PRL or testosterone. Estradiol resulted in a 72% reduction of PRL binding in the prostate, after 10 days, which subsequent PRL completely restored. PRL also partially restored the estradiol-induced time-dependent weight reduction of the prostate, but PRL coadministered from day 1 of estradiol did not inhibit the estradiol effects, suggesting a competitive mechanism for the two. While testosterone more than doubled PRL binding in the seminal vesicle, estradiol reduced it by 32% and organ weight by 21%. PRL given after estradiol restored the weight loss, but not the binding, suggesting that two different mechanisms of action are involved. In the liver, coadministration of testosterone with PRL could not inhibit the induction by PRL of its own hepatic sites, in keeping with a more direct site of action for PRL than for testosterone. These results demonstrate the profound effects of PRL, and of the sex steroids testosterone and estrogen, on PRL binding in the male sex glands and liver. The physiological implication of these findings on the role of PRL in male sexual function is currently being investigated.

Effect of polyamines and their oxidized derivatives on the metabolism of rat epididymal spermatozoa.

ABSTRACT Spermine and spermidine, occurring at relative high concentrations in the secretions of male sexual glands of various mammals, greatly stimulated the fructolysis in rat epididymal spermatozoa. Calcium likewise had a stimulatory effect on fructolysis producing together with spermine a synergistic enhancement of spermatozoa sugar utilization. While enhancing fructolysis spermine and calcium were practically without any effect on the production of 14CO2 from [2-14C]lactate. Spermatozoal fructose utilization was also markedly increased upon addition of exogenous ATP, spermine producing an additional stimulation with the latter nucleotide. In addition to spermine and spermidine, the diamines putrescine, 1,3-diaminopropane, cadaverine and histamine also significantly enhanced the formation of radioactive CO2 and lactate from uniformly labelled fructose. The stimulation of lactate formation by spermine was lost in cell free extracts of spermatozoa. This and the fact that spermine (especially in the presence of ATP) was found to stimulate the uptake of fructose by the epididymal sperm cells suggests that the polyamines interact with cell membranes facilitating sugar uptake. Oxidized spermine [N,N′-bis(3-propionaldehyde)-1,4-diaminobutane], a compound arising from the action of ruminant plasma amine oxidase, powerfully inhibited both the fructolysis and glycolysis in rat epididymal spermatozoa.

Post-mortem changes in male sex glands

In 28 of 37 cases, microscopic examination was made of male sex glands removed at autopsy and allowed to decay for up to 120 days. Special attention is drawn to the late changes caused by putrefaction. These changes are most important in forensic practice. Under the experimental conditions reported here, there are no great difficulties in the microscopic identification of male sex glands allowed to undergo putrefaction changes for up to 120 days.

Comparative pharmacological and clinical activity of 19-nortestosterone and 17-hydroxyprogesterone derivatives in man.

Studies on a comparison of the biological activity of 19-nortestosterone and 17-hydroxyprogesterone derivatives were presented. Pituitary inhibiting androgenic and anabolic effects induced by progestational steroids in parabiotic rats were presented. Initial studies with parabiotic rats showed that these compounds produce hypertrophy of secondary male sex glands and an increase in levator ani muscle weight. The female parabiont underwent marked precocious sexual maturation. In comparing levator ani weights the 17-ethyl and 17-methyl nortestosterones were the only compounds with marked anabolic activity. Progestational steroids were rated as good to excellent in inhibition of human ovulation and in the treatment of dysmenorrhea. It was found that 17-methyl-19-nortestosterone appeared to be undesirably androgenic in many women while 17-ethyl-19-nortestosterone showed good anabolic activity with minimal androgenic effects.

The Leydigcell homologue in certain teleost fishes.

THE male sex gland of the Craniata is, like other endocrine organs, extremely ancient in origin. It occurs in the Agnatha (for example, Petromyzon) and throughout the gnathostome series with relatively little recorded variation except in the Urodela. With the above exception, and another about to be described, the interstitial gland is characteristically composed of aggregations of modified connective tissue cells which occupy interstices between the seminiferous tubules of the testis. These secretory Leydig cells have a generally similar appearance, and exhibit certain common histochemical properties, in both jawless fishes and, for example, man. The interstitial aggregation of Leydig cells may constitute either a permanent secretory unit (as in most mammals) or may be renewed at the end of each breeding rhythm as in seasonal birds1.

The Male Sex Glands

The Male Sex Glands

On the relation between the male sexual gland and the experimental arteriosclerosis : II. Report Researches after Adler-Reimann's method about the function of the reticuloendothelial system

On the relation between the male sexual gland and the experimental arteriosclerosis : II. Report Researches after Adler-Reimann's method about the function of the reticuloendothelial system

On the relation between the male sexual gland and the experimental arteriosclerosis. : I. Report. Comparative studies among the experimental arteriosclerosis caused by the Lanolin feeding, the Adrenalin injection and the Vitamin D overfeeding.

On the relation between the male sexual gland and the experimental arteriosclerosis. : I. Report. Comparative studies among the experimental arteriosclerosis caused by the Lanolin feeding, the Adrenalin injection and the Vitamin D overfeeding.

Antihormonal sterilization of female animals. (1) By preparations from male sexual glands: Magistris, H.: Rev. Soc. Argent. de biol. 10: 179, 1934

Antihormonal sterilization of female animals. (1) By preparations from male sexual glands: Magistris, H.: Rev. Soc. Argent. de biol. 10: 179, 1934

Synergistic Effect of Anterior Pituitary and Male Hormone

The sex hormones of the anterior pituitary are not sex specific, but stimulate the secretion of the male as well as the female sex glands. However, for the same dose of hormone the effect on the female is far more striking than the effect on the male. In connection with other work in this laboratory, and prompted by the recent work of Funk and Harrow,1 we carried out experiments to increase the stimulating effect of the anterior pituitary hormone on the male sex glands by simultaneous injections of male hormone.These experiments were done on our laboratory albino rats. Eight rats of approximately equal age and weight were divided into 4 groups of 2 each; (1) control; (2) injected with anterior pituitary hormone; (3) injected with male hormone; (4) injected with both anterior pituitary and male hormone. All injections were made intramuscularly and twice daily. At autopsy the whole genital tract was exposed and the seminal vesicles and testes inspected macroscopically, and weighed.The solution of the anteri...