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Paul M D Foster - One of the best experts on this subject based on the ideXlab platform.
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critical window of Male Reproductive Tract development in rats following gestational exposure to di n butyl phthalate
Birth Defects Research Part B-developmental and Reproductive Toxicology, 2005Co-Authors: Christina M Carruthers, Paul M D FosterAbstract:BACKGROUND: Gestational exposure to di-n-butyl phthalate (DBP), a ubiquitous environmental contaminant, has been shown to interfere with the development of the Male Reproductive Tract by acting as an antiandrogen. This study was conducted to identify the critical days for the abnormal development of the Male Reproductive Tract, specifically the testis and epididymis. METHODS: Timed-pregnant Sprague-Dawley rats were dosed with DBP at 500 mg/kg/day on gestation day (GD) 14 and 15, 15 and 16, 16 and 17, 17 and 18, 18 and 19, or 19 and 20 (GD 0=plug day). Anogenital distance (AGD) was measured on postnatal day (PND) 1 and 13, while areloa number was recorded on PND 13 only. After weaning, Males were allowed to mature to PND 90 at which time they were necropsied. Areloa number and AGD were recorded and testes, epididymides, seminal vesicles, prostate gland, kidneys, and liver weighed. Blood serum was collected and assayed for total testosterone concentration. RESULTS: There were no observable effects on litter size, sex ratio, serum testosterone concentration, or mortality of pups. Statistically significant permanent reductions in AGD were seen in Males exposed prenatally to DBP on GD 15 and 16 or GD 18 and 19. On PND 13, areola were present in Males exposed to DBP on GD 15 and 16, 16 and 17, 17 and 18, and 19 and 20. However, permanent retention occurred only in Males after DBP exposure on GD 16 and 17. Exposure to DBP on only GD 17 and 18 elicited a reduction in epididymal weights; while exposure on only GD 16 and 17 caused a significant increase in the weights of the testes due to edema. In this study, epididymal and testicular malformations were most prevalent after exposure to DBP on any gestational day. Epididymal malformations, characterized by agenesis of various regions and small or flaccid testes were significantly increased in DBP-exposed Males only on GD 16 and 17. CONCLUSIONS: These findings suggest that 2-day DBP exposure is highly detrimental to the developing Reproductive Tract of the Male fetus and the critical window for abnormal development is GD 16–18. Birth Defects Res B 74:277–285, 2005. Published 2005 Wiley-Liss, Inc.
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Male Reproductive Tract lesions at 6 12 and 18 months of age following in utero exposure to di n butyl phthalate
Toxicologic Pathology, 2004Co-Authors: Norman J Barlow, Barry S Mcintyre, Paul M D FosterAbstract:In utero exposure of Male rats to the antiandrogen di(n-butyl) phthalate (DBP) leads to decreased anogenital distance (AGD) on postnatal day (PND) 1, increased areolae retention on PND 13, malformations in the Male Reproductive Tract, and histologic testicular lesions including marked seminiferous epithelial degeneration and a low incidence of Leydig cell (LC) adenomas on PND 90. One objective of this study was to determine the incidence and persistence of decreased AGD, increased areolae retention, and LC adenomas in adult rats following in utero DBP exposure. A second objective was to determine whether AGD and areolae retention during the early postnatal period are associated with lesions in the Male Reproductive Tract. Pregnant Crl:CD(SD)BR rats were gavaged with corn oil or DBP at 100 or 500 mg/kg/day, 10 dams per group. Three replicates of rats (n = 30 rats per replicate) were exposed from gestation day 12 to 21 and the Male offspring allowed to mature to 6, 12, or 18 months of age. Gross malformations in the Male Reproductive Tract and histologic lesions in the testes were similar to those previously described. However, testicular dysgenesis, a lesion of proliferating LCs and aberrant tubules that has not been previously described in DBP-exposed testes, was diagnosed. The incidence of this lesion was approximately 20% unilateral and 7‐18% bilateral in the high-dose group and was similar among all ages examined, implicating a developmental alteration rather than an age-related change. AGD and areolae retention were found to be permanent changes following in utero exposure to 500 mg/kg/day of DBP. Decreased AGD was a sensitive predictor of lesions in the Male Reproductive Tract, relatively small changes in AGD were associated with a significant incidence of Male Reproductive malformations. In utero DBP exposure induced proliferative developmental lesions, some of which would have been diagnosed as LC adenomas by the morphological criteria set forth by the Society of Toxicologic Pathology. However, these lesions were dissimilar to traditional LC adenomas as the LCs were poorly differentiated and the lesions contained aberrant seminiferous tubules. While the morphology and incidence of this DBP-induced testicular developmental lesion has been fully characterized by this study, the detailed pathogenesis warrants further investigation.
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pathogenesis of Male Reproductive Tract lesions from gestation through adulthood following in utero exposure to di n butyl phthalate
Toxicologic Pathology, 2003Co-Authors: Norman J Barlow, Paul M D FosterAbstract:Di(n-butyl) phthalate (DBP) acts as an antiandrogen by decreasing fetal testicular testosterone synthesis when Male rats are exposed in utero. DBP-exposed Male rats develop malformations of the Reproductive Tract secondary to the reduced fetal androgen levels. However, these malformations and the associated histologic lesions have only been described in adult rats. The objective of this study was to describe the Male Reproductive Tract lesions in fetal, early postnatal, and young adult Male rats following DBP exposure in utero. Pregnant Sprague-Dawley rats were exposed to 500 mg/kg/day DBP by gavage on gestation days (GD) 12 to 21. Male Reproductive Tracts were examined on GD 16 to 21 and on postnatal days (PND) 3, 7, 16, 21, 45, and 70. In the fetal testes, large aggregates of Leydig cells, multinucleated gonocytes, and increased numbers of gonocytes were first detected on GD 17 and increased in incidence to 100% by GD 20 and 21. These lesions resolved during the early postnatal period, while decreased numbers of spermatocytes were noted on PND 16 and 21. On PND 45, there was mild degeneration of the seminiferous epithelium, which progressed to severe seminiferous epithelial degeneration on PND 70. On PND 70, the degeneration was concurrent with ipsilateral malformed epididymides, which caused obstruction of testicular fluid flow and secondary pressure atrophy in the seminiferous tubules. In the fetus, the epididymal lesion was observed as decreased coiling of the epididymal duct. The decreased coiling progressed into the early postnatal period and adulthood, at which time malformed epididymides were apparent. As the animals were only dosed in utero, these findings indicate that DBP can initiate fetal testicular and epididymal changes that may not manifest as clear malformations until adulthood. The pathogenesis of lesion development from the fetus to the adult is important for comparison of antiandrogens with differing modes of action.
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Male Reproductive Tract malformations in rats following gestational and lactational exposure to di n butyl phthalate an antiandrogenic mechanism
Toxicological Sciences, 1998Co-Authors: Eve Mylchreest, Russell C Cattley, Paul M D FosterAbstract:Di(n-butyl) phthalate (DBP), a widely used plasticizer suspected of having estrogenic properties, was investigated for its effects on the prenatal and early neonatal development of the Reproductive Tract. Pregnant CD rats (n= 10) were given DBP at 0, 250, 500, or 750 mg/kg/day (p.o.) throughout pregnancy and lactation until their offspring were at postnatal day 20. Maternal body weights throughout the dosing period were comparable in all groups. At 750 mg/kg/day, the number of live pups per litter at birth was decreased and maternal effects on pregnancy and postimplantation loss are likely to have occurred. Anogenital distance was decreased at birth in the Male offspring at 500 and 750 mg/kg/day. The epididymis was absent or underdeveloped in 9, 50, and 71% of adult offspring (100 days old) at 250, 500, and 750 mg/kg/day, respectively, and was associated with testicular atrophy and widespread germ cell loss. Hypospadias occurred in 3, 21, and 43% of Males and ectopic or absent testes in 3, 6, and 29% of Males at 250, 500, and 750 mg/kg/day, respectively. Absence of prostate gland and seminal vesicles as well as small testes and seminal vesicles were noted at 500 and 750 mg/kg/day. Vaginal opening and estrous cyclicity, both estrogen-dependent events, were not affected in the feMale offspring, although low incidences of Reproductive Tract malformations were observed at 500 and 750 mg/kg/day. In the Male offspring, DBP produced the same spectrum of effects elicited by the antiandrogen flutamide. Thus, DBP specifically impaired the androgen-dependent development of the Male Reproductive Tract, suggesting that DBP is not estrogenic but antiandrogenic in the rat at these high dose levels. For human risk assessment, determining if this toxicity is metabolite-mediated will be critical, since marked species differences in metabolism exist.
Suresh Yenugu - One of the best experts on this subject based on the ideXlab platform.
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uroplakin expression in the Male Reproductive Tract of rat
General and Comparative Endocrinology, 2019Co-Authors: Suresh Babu Munipalli, Suresh YenuguAbstract:AbsTract Uroplakins (UPKs) play an important role in the normal and pathophysiology of the urothelium. They protect the urothelium and play a crucial role during urothelial infections by Uropathogenic E. coli. However, their functions beyond this organ system remain unexplored. A wide variety of proteins secreted in the Male Reproductive Tract tissues contribute to spermatogenesis, sperm maturation, fertilization and innate immunity. However, the presence of UPKs and their possible contribution to the Male Reproductive Tract physiology is not yet reported. Hence, in this study, we characterized UPKs in the Male Reproductive Tract of rats. To the best of our knowledge, for the first time, we report the expression of UPKs in the Male Reproductive system. Upk1a, Upk1b, Upk2 and Upk3b mRNA and their corresponding proteins were abundantly expressed in the caput, cauda, testis, seminal vesicles and the prostate. Their expression was not developmentally regulated. UPK protein expression was also localized on the spermatozoa, suggesting a role for these proteins in sperm function. To study the role of UPKs in innate immunity, Upk mRNA expression in response to endotoxin challenge was evaluated in vitro and in vivo. In the rat testicular and epididymal cell lines, Upk mRNA levels increased in response to lipopolysaccharide challenge. However, in the caput, cauda, testes, seminal vesicle and prostate obtained from LPS treated rats, Upk mRNA expression was significantly reduced. Results of this study indicate a role for UPKs in Male Reproductive physiology and innate immune responses.
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allethrin induced toxicity in the Male Reproductive Tract of rats contributes to disruption in the transcription of genes involved in germ cell production
Environmental Toxicology, 2013Co-Authors: Golla Madhubabu, Suresh YenuguAbstract:Pyrethroids are known to be neurotoxic. However, their toxic effects including that of allethrin on the Male Reproductive Tract are not elucidated. Adult Male rats were treated orally with 25, 50, 100, and 150 mg/kg body weight allethrin every day for 60 days. Lipid peroxidation was increased (p < 0.001) in the caput, cauda, and testes. Nitric oxide production was increased (p < 0.001) in the caput, but unaltered in the cauda and testes. The activities of catalase, glutathione peroxidase, glutathione-S-transferase, and superoxide dismutase were decreased in the caput and cauda where as a decrease was observed in the testis obtained from allethrin treated rats. In the epididymides and testes, damage to tubular architecture, congestion, degeneration of epithelial cell lining, intestinal edema, and presence of dead or degenerating spermatids were observed in a dose dependent manner. The expression profile of genes involved in spermatogenesis (Tgf-beta1), sperm maturation (Spag11e), and sperm function (Defb22) were reduced (p < 0.001) in allethrin rats. The expression of p53 gene was decreased and increased phosphorylation of MAPK (p42/p44) expression was observed the Male Reproductive Tract tissues of allethrin treated rats. Although earlier studies have reported the effects of allethrin inhalation because of the use of mosquito coils and vaporizers, our results for the first time prove that oral exposure to allethrin could affect fertility and may contribute to deregulation of cell cycle in the Male Reproductive Tract. © 2013 Wiley Periodicals, Inc. Environ Toxicol 29: 1330–1345, 2014.
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effect of continuous inhalation of allethrin based mosquito coil smoke in the Male Reproductive Tract of rats
Inhalation Toxicology, 2012Co-Authors: Golla Madhubabu, Suresh YenuguAbstract:Objectives: Continuous inhalation of allethrin-based mosquito coil smoke may affect fertility, an aspect that has not received much attention. In this study, we attempt to understand the harmful effects on the Male Reproductive system caused by continuous exposure to allethrin-based mosquito coil smoke.Methods: Adult Wistar rats were allowed to inhale mosquito coil smoke for 15–180 days, and Male Reproductive Tract tissues (caput, cauda, and testes) were collected. Using standard biochemical techniques, changes in oxidative stress (lipid peroxidation) and antioxidant status was measured. Histopathological analyses were carried out to assess pathomorphological damage in the caput, cauda, and testis. Real-time polymerase chain reaction was carried out to determine the expression pattern of the stress-response gene, p53, and the spermatogenic factors c-Kit, Scf, and Tgf-β1.Results: In rats exposed to allethrin-based mosquito coil smoke for 15–180 days, compared to the unexposed controls, lipid peroxidation w...
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differential expression and antibacterial activity of epididymis protein 2 isoforms in the Male Reproductive Tract of human and rhesus monkey macaca mulatta
Biology of Reproduction, 2004Co-Authors: Maria Christina W Avellar, Suresh Yenugu, Luciana Honda, Katherine G Hamil, Gail Grossman, Peter Petrusz, Frank S French, Susan H HallAbstract:The epididymis protein 2 (EP2) gene, the fusion of two ancestral b-defensin genes, is highly expressed in the epididymis and subject to species-specific regulation at the levels of promoter selection, transcription, and mRNA splicing. EP2 mRNA expression is also androgen dependent, and at least two of the secreted proteins bind spermatozoa. Alternative splicing produces more than 17 different EP2 mRNA variants. In this article, the expression of EP2 variants was profiled in different tissues from the human and rhesus monkey (Macaca mulatta) Male Reproductive Tract using reverse transcriptase-polymerase chain reaction. Different EP2 mRNA variants were identified not only in human and rhesus testis and epididymis but also in the novel sites, seminal vesicle and prostate. Immunolocalization of EP2 protein in epithelial cells from rhesus and human seminal vesicle demonstrated that EP2 transcripts are translated in these tissues. In addition, two novel splicing variants, named EP2R and EP2S, were discovered. EP2C was the only splice variant expressed in all tissues tested from rhesus monkey. However, expression was not detected in human testis or seminal vesicle. For the first time, bactericidal function was demonstrated for EP2C, EP2K, and EP2L. Taken together, the results indicate that EP2 expression is more widespread in the Male Reproductive Tract than realized previously. Whereas the activity of every EP2 variant tested thus far is antibacterial, further investigation may reveal additional physiological roles for EP2 peptides in the primate Male Reproductive Tract.
Rex A Hess - One of the best experts on this subject based on the ideXlab platform.
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efferent duct toxicity with secondary testicular changes in rats following administration of a novel leukotriene a4 hydrolase inhibitor
Toxicologic Pathology, 2012Co-Authors: Dianne M Creasy, Rex A Hess, Elizabeth Baxter, Marcia E Pereira, Charles Johnson, Petra Vinken, Sandra S SnookAbstract:The efferent ducts represent an important site of toxicity in the Male Reproductive Tract but are not routinely examined in toxicity studies. This article describes a primary efferent duct toxicity...
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the role of estrogen in testis and the Male Reproductive Tract a review and species comparison
Animal Reproduction (AR), 2004Co-Authors: Rex A Hess, Kay CarnesAbstract:Testosterone and estrogen are hormones important to both sexes. In the adult testis, estrogen is synthesized by Leydig cells and germ cells, producing a relatively high concentration in rete testis fluid and in semen of several species. Estrogen receptors (ER) are present in the testis, efferent ductules and epididymis of most species; however, ERα is reported absent in the testis of a few, including man. ERα is abundant in the efferent ductule epithelium of every species examined to date. Its primary function is the regulated expression of proteins involved in fluid reabsorption. Disruption of ERα , either in the knockout (ERα KO) or by treatment with a pure antiestrogen, results in dilution of cauda epididymal sperm, disruption of sperm morphology, inhibition of sodium transport and subsequent water reabsorption, increased secretion of Cl - , and eventual decreased fertility. Loss of aromatase activity in the ArKO mouse does not result in an ERα KO or antiestrogen phenotype, suggesting that epithelial ERα in the efferent ductules may exhibit ligand-independent activity. In addition to the primary regulation of luminal fluid and ion transport, estrogen is also responsible for maintaining a differentiated epithelial morphology through a mechanism remaining to be discovered. Thus, estrogen or its receptor is important for Male Reproductive Tract function in numerous species.
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Estrogen in the adult Male Reproductive Tract: A review
Reproductive Biology and Endocrinology, 2003Co-Authors: Rex A HessAbstract:Testosterone and estrogen are no longer considered Male only and feMale only hormones. Both hormones are important in both sexes. It was known as early as the 1930's that developmental exposure to a high dose of estrogen causes malformation of the Male Reproductive Tract, but the early formative years of Reproductive biology as a discipline did not recognize the importance of estrogen in regulating the normal function of the adult Male Reproductive Tract. In the adult testis, estrogen is synthesized by Leydig cells and the germ cells, producing a relatively high concentration in rete testis fluid. Estrogen receptors are present in the testis, efferent ductules and epididymis of most species. However, estrogen receptor-α is reported absent in the testis of a few species, including man. Estrogen receptors are abundant in the efferent ductule epithelium, where their primary function is to regulate the expression of proteins involved in fluid reabsorption. Disruption of the α-receptor, either in the knockout (αERKO) or by treatment with a pure antiestrogen, results in dilution of cauda epididymal sperm, disruption of sperm morphology, inhibition of sodium transport and subsequent water reabsorption, increased secretion of Cl^-, and eventual decreased fertility. In addition to this primary regulation of luminal fluid and ion transport, estrogen is also responsible for maintaining a differentiated epithelial morphology. Thus, we conclude that estrogen or its α-receptor is an absolute necessity for fertility in the Male.
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oestrogen its receptors and function in the Male Reproductive Tract a review
Molecular and Cellular Endocrinology, 2001Co-Authors: Rex A Hess, David Bunick, Janice M BahrAbstract:Oestrogen is synthesized in the Male Reproductive system by at least three different cell types; Sertoli, Leydig and germ cells. Although testosterone is recognized as the primary sex steroid in man, oestrogen is produced in sizable quantities in the testis, as well as the brain and is found in extremely high concentrations in the semen of several species. The high concentration of oestrogen in rete testis fluid of the rodent is now thought to be derived from the conversion of testosterone to estradiol by P450 aromatase in germ cells of the testis and spermatozoa traversing the Reproductive Tract. This new major source of oestrogen would target oestrogen receptors in the Male Reproductive Tract, in particular the efferent ductules, which contain the highest concentration of oestrogen receptor-alpha. This recent data raises new hypotheses regarding the role of oestrogen in the function of the Male Reproductive system. The oestrogen receptor-alpha knockout mouse was used to help define the function of oestrogen in the Male. It was found that oestrogen receptor-alpha is essential for fluid reabsorption in the efferent ductules and in the absence of expression the Male is infertile.
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oestrogen in fluid transport in efferent ducts of the Male Reproductive Tract
Reviews of Reproduction, 2000Co-Authors: Rex A HessAbstract:This review focuses on the importance of oestrogen and oestrogen receptors in the Male Reproductive system, with a special interest in the newly discovered role of oestrogen in the regulation of fluid reabsorption in the efferent ductules of the testis. Early work on oestrogen synthesis indicated that Leydig and Sertoli cells were the only important cells in the production of this steroid in the adult testis. However, more recent work has shown that germ cells and spermatozoa also contain aromatase and produce oestrogen. The observation that germ cells synthesize oestrogen contributed to a new hypothesis that oestrogen in the lumen of the Male Reproductive Tract targets the epithelial lining of efferent ductules and the epididymis. The location of nuclear oestrogen receptors in the Male Reproductive Tract has also been investigated and it has been found that oestrogen receptor α is more abundant in the efferent ductules of the testis than in any other tissue of the Male or feMale. In all species examined to date, oestrogen receptor α has been found to be abundant in the efferent ductules. The structure and function of the efferent ductules are taken into account as these tubules are responsible for the reabsorption of almost 90% of the luminal rete testis fluid. Thus, it was logical to hypothesize that oestrogen receptors play a role in the regulation of fluid reabsorption in efferent ductules. The oestrogen receptor α knockout mouse was used to help define this role of the receptor in Males. In this animal model, the efferent ductules are altered markedly from a reabsorptive epithelium to a squamous epithelium devoid of lysosomes and endocytotic organelles. Although the separate roles for oestrogens and androgens in the regulation of fluid reabsorption are controversial and remain to be resolved, it is now established that loss of oestrogen receptor function in Males interferes with the resorptive function of efferent ductules, a function that is essential for fertility. Future studies will focus on the biochemical and physiological mechanisms involved in the regulation of water and ion movement by oestrogen in the Male Reproductive Tract.
Paula J Lapinskas - One of the best experts on this subject based on the ideXlab platform.
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peroxisome proliferator activated receptors mediators of phthalate ester induced effects in the Male Reproductive Tract
Toxicological Sciences, 2005Co-Authors: Christopher J Corton, Paula J LapinskasAbstract:Many phthalate ester plasticizers are classified as peroxisomeproliferators (PP), a large group of industrial and pharmaceuticalchemicals. Like PP, exposure to some phthalates increases hepato-cyteperoxisomeandcellularproliferation,aswellastheincidenceofhepatocellular adenomas in mice and rats. Most effects of PP aremediatedbythreenuclearreceptorscalledperoxisomeproliferator-activatedreceptors(PPARa,b,g).AnobligateroleforPPARainPP-inducedeventsleadingtolivercanceriswell-established.Exposureofratsinuteroorintheneonatetoasubsetofphthalateesterscausesprofound, sometimes irreversible malformations in the Male repro-ductive Tract. We review here the data that supports or discountsroles for PPARs in phthalate-induced testis toxicity including(1) toxic effects of phthalates on the Male Reproductive Tract,(2) expression of PPARs in the testis, (3) activation of PPARs byphthalates, (4) role of PPARa in testis toxicity, (5) gene targets ofphthalates involved in steroid biosynthesis and catabolism, and(6) interactions between PPARs and other nuclear receptors thatplay roles in testis development and homeostasis. Critical researchneeds are identified that will help determine the significance ofPPARs in phthalate-induced effects in the rat Male ReproductiveTract and the relevance of toxicity to humans.Key Words: phthalate ester; PPAR; testis; peroxisomeproliferator; Male Reproductive Tract.
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peroxisome proliferator activated receptors mediators of phthalate ester induced effects in the Male Reproductive Tract
Toxicological Sciences, 2005Co-Authors: Christopher J Corton, Paula J LapinskasAbstract:Many phthalate ester plasticizers are classified as peroxisome proliferators (PP), a large group of industrial and pharmaceutical chemicals. Like PP, exposure to some phthalates increases hepatocyte peroxisome and cellular proliferation, as well as the incidence of hepatocellular adenomas in mice and rats. Most effects of PP are mediated by three nuclear receptors called peroxisome proliferator-activated receptors (PPARalpha,beta,gamma). An obligate role for PPARalpha in PP-induced events leading to liver cancer is well-established. Exposure of rats in utero or in the neonate to a subset of phthalate esters causes profound, sometimes irreversible malformations in the Male Reproductive Tract. We review here the data that supports or discounts roles for PPARs in phthalate-induced testis toxicity including (1) toxic effects of phthalates on the Male Reproductive Tract, (2) expression of PPARs in the testis, (3) activation of PPARs by phthalates, (4) role of PPARalpha in testis toxicity, (5) gene targets of phthalates involved in steroid biosynthesis and catabolism, and (6) interactions between PPARs and other nuclear receptors that play roles in testis development and homeostasis. Critical research needs are identified that will help determine the significance of PPARs in phthalate-induced effects in the rat Male Reproductive Tract and the relevance of toxicity to humans.
Pedro Oliveira - One of the best experts on this subject based on the ideXlab platform.
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cftr regulation of aquaporin mediated water transport a target in Male fertility
Current Drug Targets, 2015Co-Authors: Marco G Alves, Mario Sousa, Tito T Jesus, Pedro OliveiraAbstract:The formation of competent spermatozoa is associated with the movement of large quantities of water and electrolytes in the various tissues and luminal fluids of the Male Reproductive Tract. The cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-activated Cl(-) and HCO3(-) membrane transporter. CFTR gene mutations cause cystic fibrosis (CF), the most common lethal genetic disease in Caucasians. Of note, one hallmark in CF is Male infertility. Indeed, mutations of CFTR gene cause abnormal production of germ cells and a reduction in germ cell quality and number. Compelling evidence illustrates that CFTR is involved in several pivotal processes for Male fertility, including spermatogenesis and sperm capacitation. Recent studies show that CFTR acts as a molecular partner of specific water channels, known as aquaporins, in somatic testicular cells. Aquaporins are water-selective channels that enable high permeability fluxes of water across plasma membranes. In the Male Reproductive Tract, water movements and ion concentrations are determinants for the Male Reproductive function. Therefore, aquaporins expression and function play a key role in Male fertility. Herein we present an overview of the expression and function of CFTR in the Male Reproductive Tract, highlighting the Reproductive outcomes in Male carriers of CFTR mutations and CF couples. We also present an up-to-date discussion on the expression and role of aquaporins in the Male Reproductive Tract. Finally, we discuss the regulation of aquaporin-mediated water transport by CFTR in the Male Reproductive Tract and its implication for Male fertility.
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physiology of na h exchangers in the Male Reproductive Tract relevance for Male fertility
Biology of Reproduction, 2014Co-Authors: Ana D Martins, Raquel L Bernardino, Aline Neuhausoliveira, Mario Sousa, Marco G Alves, Pedro OliveiraAbstract:The maintenance of pH homeostasis in the Male Reproductive Tract is kept through the involvement of several mechanisms, among which is included the transmembranous movement of H(+) ions. Na(+)-H(+) exchangers (SLC9, solute carrier 9 family members) are among the membrane transporters known to participate in intracellular and extracellular pH regulation but also have important roles in salt and water absorption across epithelia and in the regulation of cell volume. The presence of several Na(+)-H(+) exchangers has been reported in the Male Reproductive Tract. Their involvement in the processes that ensure the correct pursuance of the spermatogenetic event and spermatozoa maturation has been suggested. Indeed, the formation of mature spermatozoa is highly dependent on the maintenance of adequate ductal luminal milieu pH and ionic balance. Perturbations in these processes result in reduced Male Reproductive potential and consequently Male subfertility and/or infertility. Thus, it is imperative to understand H(+) transport dynamics in order to identify and counteract possible alterations associated with reduced Male fertility caused by pathological conditions. Herein, we will discuss the expression pattern and physiological roles of SLC9 family members in the cells of the Male Reproductive Tract as well as the molecular basis of H(+) transport and its involvement in Male Reproductive potential.
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physiology of na h exchangers in the Male Reproductive Tract relevance for Male fertility
Biology of Reproduction, 2014Co-Authors: Ana D Martins, Raquel L Bernardino, Aline Neuhausoliveira, Mario Sousa, Marco G Alves, Rosalia Sa, Pedro OliveiraAbstract:ABSTract The maintenance of pH homeostasis in the Male Reproductive Tract is kept through the involvement of several mechanisms, among which is included the transmembranous movement of H+ ions. Na+-H+ exchangers (SLC9, solute carrier 9 family members) are among the membrane transporters known to participate in intracellular and extracellular pH regulation but also have important roles in salt and water absorption across epithelia and in the regulation of cell volume. The presence of several Na+-H+ exchangers has been reported in the Male Reproductive Tract. Their involvement in the processes that ensure the correct pursuance of the spermatogenetic event and spermatozoa maturation has been suggested. Indeed, the formation of mature spermatozoa is highly dependent on the maintenance of adequate ductal luminal milieu pH and ionic balance. Perturbations in these processes result in reduced Male Reproductive potential and consequently Male subfertility and/or infertility. Thus, it is imperative to understand H...