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Introducción: las infecciones del tracto urogenital son una de las causas más frecuentes durante las consultas por infertilidad masculina. Comúnmente se evalúan aquellas causadas por bacterias y virus, mientras que las producidas por hongos han sido subvaloradas; sin embargo, en las últimas décadas su frecuencia ha aumentado. Objetivo: describir algunas micosis del tracto urogenital masculino y su posible efecto sobre la fertilidad. Materiales y métodos: se realizó una revisión sistemática de la literatura publicada sobre las micosis del tracto urogenital masculino y la fertilidad en las bases de datos PubMed, ScienceDirect, SciELO, Redalyc, Springer y Google Académico. Resultados: se encontraron un total de 3.426 publicaciones que hablaban sobre el tema. Entre la información revisada se comprobó que el 90% de las micosis reportadas en el tracto urogenital masculino son ocasionadas por Candida spp., Aspergillus spp., Cryptococcus spp. y Coccidioides spp., microorganismos que podrían ser los causantes de uretritis, balanopostitis, úlceras, pseudotumores, orquitis y prostatitis; además de afectar negativamente la calidad espermática, lo que causa alteraciones en la fecundación. Conclusiones: las infecciones fúngicas del tracto urogenital pueden desatar infertilidad, que si se tratan correctamente disminuirán la diseminación, morbilidad y mortalidad a causa de estos microrganismos.

The review covers the data on the toxic effects of trace elements on the male reproductive system. The basic pathogenetic mechanisms of male infertility are described. Different points of view on the effect of high concentrations of trace elements on the functions of endocrine system components, male reproductive tract, properties of gametes, and state of their genetic material are considered.

Human and wildlife exposure to chemicals is thought to be extensive and particularly to endocrine-disrupting chemicals (EDCs) suspected to alter male reproductive tract. When the exposure occurs during perinatal period (fetal, neonatal periods or puberty) the reproductive health alterations are irreversible suggesting a developmental origin to male infertility. This concept is supported by numerous epidemiologic and experimental studies. This review summarizes the data concerning the epigenetic mechanisms (DNA methylation, chromatin remodelling, small-non coding RNAs) involved in developmentally-induced male infertility. These data open potentially to new diagnosis tools and new trails to assessment of EDCs risks.

e15659 Background: The incidence of cancer among the people of reproductive age is constantly increasing. Although FGF2/FGFR2 expression in the male reproductive tract has been reported, there is no evidence of the impact of FGFRs inhibitors on sperm function. Therefore, the objective of this large study was to determine the effects of alofanib, selective FGFR2 allosteric extracellular inhibitor on the regulation of sperm physiology using the rat and rabbit models. Methods: Two-hundred forty Sprague-Dawley rats and 30 Chinchilla white rabbits received alofanib (0–40.5 and 0–21.6 mg/kg/day, respectively) intravenously on a consecutive daily dosing schedule for six months. Eighty rats and 8 rabbits were in the control group. The subchronic study evaluated high doses (300 mg/kg/day) of alofanib for 2 months in 15 male rats. Necropsy was conducted following treatment/recovery periods, and histologic examinations were performed. Results: Animals were active. After injections of a dose equivalent to a human therapeutic dose during 6 months, most of the seminiferous tubules were empty, the elements of spermatogenesis were not classified, and altered primary spermatogonia and spermatocytes were distinguished in male rats. After injections of a five-fold dose, all seminiferous tubules were empty and expelled by a cylindrical epithelium. Very similar changes in sperm physiology were founded in rabbits. Most of the seminiferous tubules were blank, and some tubules contained eosinophilic amorphous masses. High doses of alofanib resulted in pronounced atrophy of the spermatogenic tubule epithelium. Multinucleated giant cells were observed in the lumen of a part of the tubules. There were no changes in untreated animals. Conclusions: FGFR2 inhibition led to the suppression of spermatogenesis. Male cancer patients should be informed of this potential adverse event before treatment with FGFR2 inhibitors.

There is an increasing frequency of reports regarding the persistence of the Ebola virus (EBOV) in Ebola virus disease (EVD) survivors. During the 2014–2016 West African EVD epidemic, sporadic transmission events resulted in the initiation of new chains of human-to-human transmission. Multiple reports strongly suggest that these re-emergences were linked to persistent EBOV infections and included sexual transmission from EVD survivors. Asymptomatic infection and long-term viral persistence in EVD survivors could result in incidental introductions of the Ebola virus in new geographic regions and raise important national and local public health concerns. Alarmingly, although the persistence of filoviruses and their potential for sexual transmission have been documented since the emergence of such viruses in 1967, there is limited knowledge regarding the events that result in filovirus transmission to, and persistence within, the male reproductive tract. Asymptomatic infection and long-term viral persistence in male EVD survivors could lead to incidental transfer of EBOV to new geographic regions, thereby generating widespread outbreaks that constitute a significant threat to national and global public health. Here, we review filovirus testicular persistence and discuss the current state of knowledge regarding the rates of persistence in male survivors, and mechanisms underlying reproductive tract localization and sexual transmission.

The spermatogenesis is the process by which spermatozoa are generated in the testes. The spermatozoa travel male reproductive tract during which they meet many substances secreted from reproductive organs. One of the substances is epididymal protease inhibitor (EPPIN) that is involved in the post-testicular maturation including capability of fertilizing the eggs. The expression of EPPIN gene was investigated in various tissues of sexually mature and regressed male Syrian hamsters by reverse transcription polymerase chain reaction (RT-PCR). The EPPIN gene was identified in the testis and epididymis of the male Syrian hamsters and compared to the genes reported previously. There was no expression of EPPIN gene in reproductively and completely regressed testes of Syrian hamster. These results suggest that the expressions of the EPPIN gene are associated with the reproductive capability in the Syrian hamsters.

Arthropod-borne viruses (arboviruses) are resurging across the globe. Zika virus (ZIKV) has caused significant concern in recent years because it can lead to congenital malformations in babies and Guillain-Barré syndrome in adults. Unlike other arboviruses, ZIKV can be sexually transmitted and may persist in the male reproductive tract. There is limited information regarding the impact of ZIKV on male reproductive health and fertility. Understanding the mechanisms that underlie persistent ZIKV infections in men is critical to developing effective vaccines and therapies. Mouse and macaque models have begun to unravel the pathogenesis of ZIKV infection in the male reproductive tract, with the testes and prostate gland implicated as potential reservoirs for persistent ZIKV infection. Here, we summarize current knowledge regarding the pathogenesis of ZIKV in the male reproductive tract, the development of animal models to study ZIKV infection at this site, and prospects for vaccines and therapeutics against persistent ZIKV infection.

Reproductive tract inflammation and infection are a common cause of male infertility, with a prevalence of 6%-10% on male infertile population. Infections can affect different sites of the male reproductive tract, such as the testis, epididymis and male accessory sex glands. In the chapter are summarized the most important infections and inflammatory diseases associated with male infertility and their treatment.

The prostate is a secretory organ of the male reproductive tract. The prostate is located below the urinary bladder surrounding the urethra. The development of the prostate as well as its adult function is dependent upon the presence of testicular androgens. The organ is the source of three important disease conditions, prostate cancer, benign prostatic hyperplasia (BPH) and prostatitis.

Movement of water into and out of the cell is fundamental to life. In the male reproductive tract, at the level of the seminiferous epithelium, Sertoli cells are pivotal in mediating the movement of water into the luminal compartment, a process providing a means of transport of spermatozoa into the epididymal ducts. Here, we describe a stopped-flow light-scattering methodology to easily assess the Sertoli cell osmotic water permeability. The devised methodology is well suited for studying how the Sertoli cell's permeability changes following exogenous stimuli.

The development of human penis is affected by hormones from the very beginning of life. At an early stage in embryonic development, both sexes possess equivalent internal structures. These are the mesonephric ducts and paramesonephric ducts. The presence of the SRY gene on the Y chromosome causes the development of the testes in males, and the subsequent release of hormones which cause the paramesonephric ducts to regress.

Environmental estrogens including trace contaminants and phytoestrogens have been classified as endocrine disruptors (EDs), and it is hypothesized that ED compounds may be etiologic agents in male reproductive tract problems and breast cancer in women. It is clear from experimental studies that industrial estrogenic compounds (xenoestrogens) such as bisphenol A and phytoestrogens are selective estrogen receptor modulators (SERMs) that may exhibit structure-dependent and tissue-specific estrogenic or antiestrogenic activities. However, to date there is minimal evidence showing that ED compounds are causal factors in breast cancer, male reproductive tract problems such as decreased sperm counts and fertility, or prostate and testicular cancers. Moreover, many of the so-called global male reproductive problems, such as decreased sperm counts, are currently not recognized as global problems and may be due to unidentified regional problems including obesity.

Transport of sperm through the male reproductive tract and then the upper female reproductive tract is the major function of seminal vesicle gland fluid. Seminal vesicle glands are a paired structure and a major accessory sex organ in most species. Seminal vesicle glands contribute to the secretions that make up the volume of semen. These secretions are required to maintain sperm viability and function on their journey to the ovum to facilitate fertilization. There is evidence to suggest a secondary role for seminal vesicle gland fluid in facilitating communication between the dam and sire at the time of copulation. This article describes (1) fetal development of the seminal vesicle glands, (2) the seminal vesicle gland specific secretions, and (3) the function of the seminal vesicle gland secretions as they pertain to mammalian reproduction.

The human penile erection progresses from a spongy-soft to a bony-rigid state, which results from a seamless interplay between penile structures. The tunical outer longitudinal layer and intracavernosal pillars are essential structures for erection rigidity. Once an episodic parasympathetic activity overrides the basal sympathetic tone, erections result from increased arterial inflow, sinusoidal trapping, and decreased venous drainage of the corpora cavernosa secondary to nitric oxide activities which relax the smooth muscles. Detumescence ensues following smooth muscle contraction mediated by a sympathetic surge such as ejaculation. Tumescence (but not rigidity) occurs in the corpus spongiosum and glans penis, where neither intracavernosal pillar nor tunical outer longitudinal layer presents.

The human penis consists of two corpora cavernosa and one corpus spongiosum whereby the urethra resides centrally and the glans penis caps distally. Its anatomy clings to the pelvic wall so tenaciously that sexual and urinary passage function work perfectly. A dual penile vascular system is indispensable to the corpora cavernosa, which are encompassed by the tunica albuginea's bi-layered structure, expressed as a 360 degrees inner circular and a 300 degrees outer longitudinal coat. The erection-related veins include one deep dorsal, two cavernosal, and four para-arterial veins (PAVs). A fibroskeleton is critical for facilitating erectile rigidity, which is further supported by the distal ligament.

The seminal vesicle is the largest male accessory sex gland and makes the greatest contribution to the seminal plasma in most mammalian species, including human. Factors secreted from the seminal vesicle facilitate reproduction in two ways. Firstly, they assist in delivery of the sperm into the female reproductive tract and promote sperm retention, viability and function during transit of sperm to the site of fertilization. Secondly, seminal vesicle secretions interact with female tissues after coitus to influence female reproductive physiology and improve the chances of conception, embryo development and reproductive success.

Cell integration between the immune and reproductive systems is the basis for normal male reproductive physiology. Cytokines are a part of the autocrine/paracrine network operating in the male reproductive tract. At the same time, immunological reactions occurring via cytokines appear to be both beneficial and/or risk factors for male fertility. As the cytokines are produced by a whole spectrum of cells in all compartments of the male genital tract, they can also be involved in a variety of andrological disorders. The monitoring of cytokines and other immune factors in seminal plasma may offer a chance to better understand the mechanisms leading to sub-/infertility. In this review, we present insights into cytokine interplay in some of the pathological conditions associated with male reproduction.

Male reproductive tract infections (MRTIs) are very common diseases of the genital system. In this chapter we will summarize the last clinical updates on epididimitys, orchitis, prostatitis and on a very severe infection such as the Fournier’s Gangrene. Our goal is also focusing on the pratical role of imaging in relation to the differencial diagnosis of those diseases.

The sexual differentiation paradigm contends that the female pattern of the reproductive system is established by default, as the male reproductive tracts (Wolffian ducts) in the female degenerate due to a lack of androgen. Here, we discovered that female mouse embryos lacking Coup-tfII in the Wolffian duct mesenchyme became intersex that contained both female and male reproductive tracts. Retention of Wolffian ducts was not caused by ectopic androgen production or action. Instead, enhanced p-ERK signaling in Wolffian duct epithelium was responsible for the retention in an androgen-independent manner. These results support our hypothesis that elimination of Wolffian ducts in female embryos is actively promoted by COUP-TFII, which suppresses a mesenchyme-epithelium crosstalk responsible for Wolffian duct maintenance.

Prostatic disease is common in dogs but rare in cats. In the dog, prostatic disease is the most common disorder of the male reproductive tract. Diseases of the prostate gland include benign prostatic hyperplasia, cystic benign prostatic hyperplasia; squamous metaplasia, paraprostatic cysts; infectious prostatic abcessation and prostatic neoplasia. This chapter discusses anatomy, physiology, diagnostic tests and prostatic disorders.

This article provides an overview of infectious and inflammatory conditions associated with male infertility. These conditions may affect several components of the male reproductive tract and therefore have the ability to potentially alter sperm function. The effect of these conditions on male fertility is poorly understood and often underestimated.

The ejaculate composition is extremely complicated and variable among livestock species. The seminal proteins and enzymes are vital for ejaculate metabolism, spermatozoa performance, survival, and transport within the feminine reproductive tract. Proteases and proteinase inhibitors are secreted by the accessory sex glands of the male reproductive tract and find mixed with the spermatozoa throughout ejaculation. But an entire understanding of those enzymes and their per- formance in numerous class species is not obtainable. The performance of the assorted proteinases and protease inhibitors of ejaculate stay a mystery, and only a few studies are conducted concerning the characterization of those enzymes. Throughout this review, we tend to target the current un - derstanding of the key proteases and their inhibitors of ejaculate from various mammalian species.

The study of pathological conditions of the male reproductive system is paramount to understanding reproductive inefficiency in the Sahel goat. In this study, 1048 Sahel bucks presented for slaughter at the Maiduguri metropolitan abattoir were evaluated for the presence of various pathological abnormalities of the reproductive system. A total incidence of 15.08% was recorded for various pathological conditions, with testicular, penile, and scrotal conditions having incidences of 7.82%, 4.80 and 2.50%, respectively. Bilateral testicular hypoplasia and atrophy and unilateral cryptorchidism accounted for incidences of 4.10%, 2.38%, and 1.24%, respectively, while paraphimosis and scrotal laceration had incidences of 1.72% and 1.05%, respectively. Age specific incidence of pathological conditions were not significant(P>0.05)between bucks aged (P<0.05)incidence of pathological conditions than other age groups. Histopathological evidence of inflammation, degeneration, and atrophy was observed in the testes, while inflammatory changes were observed in the prepuce.

Immunobiological changes in spermatozoa within the male reproductive tract are vital for their viability, and hence for reproductive efficiency. The secretions of the seminal vesicles have immunosuppressive property that attenuates the antigenic effects of spermatozoa in the male reproductive tract. However, when spermatozoa find a way to outside of the rete testis or epididymis due to trauma or infection, they can cause significant inflammatory and immunological reactions in the surrounding tissues. This has also been observed in the female reproductive tract. However, such cases are rare and the reason for this is unknown. Antisperm antibodies are the main cause of infertility in humans. The purpose of this review is to analyze these immunobiological changes from the time of spermatozoa formation in rete testis to their role in fertilizing the oocytes in the female reproductive tract.

The α-(1,2) fucosyltransferases (Fut1 and Fut2) and α-(1,3) fucosyltransferases (Fut4, Fut9) are responsible for the synthesis of Lewis X (LeX) and Lewis Y (LeY) conjugated to glycoproteins. We recently reported that these fucosyltransferases were differentially expressed in the reproductive tract of male mouse. Here, we studied the effect of androgen on fucosyltransferase expression through the use of mouse castration models. We found that Fut1 mRNA and Fut4 mRNA were upregulated, while Fut2 mRNA and Fut9 mRNA were downregulated by androgen in the caput epididymis. However, in the vas deferens and prostate, only Fut4 mRNA and Fut2 mRNA were respectively upregulated following exposure to androgen. In the seminal vesicle, all fucosyltransferases, with the exception of Fut9, were upregulated. We identified the androgen receptor binding sites (ARBSs) of Fut2, Fut4 and Fut9 in the caput epididymis. Luciferase assay for these ARBSs is able to provide an indication as to why Fut4 and Fut9 are differently expressed and regulated by androgen, although they catalyze the same α-(1,3) fucose linkage. Our study showed that androgen could differentially regulate the expression of these fucosyltransferases and provided an insight into the characteristic distribution of each fucosyltransferase responsible for LeX/LeY biosynthesis in the male reproductive tract.

The effects of male-derived extracts on female receptivity to remating were investigated in Trigonotylus caelestialium (Kirkaldy) (Heteroptera: Miridae). The aqueous extracts of male reproductive tracts were observed to reduce receptivity both at 3 h and at 1 d after injection into the abdomens of females. Next, ultrafiltration was used to divide the aqueous extracts of the male reproductive tracts into three molecular-weight (MW) fractions: 14 kDa. The filtrate containing the MW substances 14 kDa inhibited receptivity at 1 and 2 d after injection. Finally, the male reproductive tract organs were divided into the accessory glands, testes, and the remaining reproductive organs, including the seminal vesicles. Aqueous extracts of the accessory glands reduced the receptivity of females both at 3 h and 2 d after injection, whereas those of the testes decreased the receptivity of females at 3 h after injection. Together, the results indicate that more than one mechanism may be involved in the effects of male-derived substances on female receptivity in T. caelestialium. The findings suggest that low-MW male-derived substances in the accessory glands and testes cause short-term inhibition and that the high-MW substances in the accessory gland inhibit female mating at a later period.

The mammalian epididymis plays a role in sperm maturation through its secretory activity. Among the proteins secreted by the epithelium, there are significant amounts of acid hydrolases. In most cell types, the normal distribution of lysosomal enzymes is mediated by mannose-6-phosphate receptors (MPRs). In this study, we analysed the expression and distribution of the cation-dependent MPR (CD-MPR) in epididymis from control, castrated or castrated rats with testosterone replacement. It was observed that expression of CD-MPR increased due to castration in all regions of the epididymis, which was reversed by injection of testosterone. We also measured the activity of α-mannosidase and observed that the castration tends to increase the retention of this enzyme in the tissue, which is reversed by the hormone replacement. In corpus, this resulted in a reduced secretion of the enzyme. Immunohistochemistry showed that CD-MPR has a supranuclear location (different from the cation-independent MPR), most likely in principal cells, and low reactivity in other cell types. The signal in castrated animals was more intense and tended to redistribute towards the apical cytoplasm. Thus, we concluded that expression and distribution of CD-MPR is affected by decrease of testosterone in rat epididymis, and this could change the distribution of lysosomal enzymes.