scholarly journals Phthalate Toxicity in Rats and Its Relation to Testicular Dysgenesis Syndrome in Humans

2021 ◽  
pp. 019262332110453
Author(s):  
Cynthia J. Willson
Keyword(s):  
Reproductive Tract ◽  
Normal Development ◽  
Environmental Chemicals ◽  
Testicular Development ◽  
Reproductive Disorders ◽  
Male Reproductive Tract ◽  
Testicular Dysgenesis Syndrome ◽  
Human Male ◽  
Testicular Dysgenesis ◽  
Common Etiology

This work describes the relevance of toxicology studies of environmental chemicals, with a focus on phthalates, for a hypothesis that certain human male reproductive disorders and diseases have a common etiology of disturbance of normal development in utero. The “Testicular Dysgenesis Syndrome” hypothesis in humans has parallels in male reproductive tract abnormalities and microscopic lesions reported for phthalate toxicity in rats. Additionally, this work describes the histological findings of abnormal testicular development (testicular dysgenesis) in rats as compared to those in humans, as well as potential findings in rats at different ages, from the embryo to the adult.

scholarly journals Environmental anti-androgens and male reproductive health: focus on phthalates and testicular dysgenesis syndrome

Reproduction ◽  
2004 ◽  
Vol 127 (3) ◽  
pp. 305-315 ◽  
Author(s):  
Jane S Fisher
Keyword(s):  
Reproductive Health ◽  
Reproductive Tract ◽  
Semen Quality ◽  
Phthalate Esters ◽  
Male Reproductive Tract ◽  
Testicular Dysgenesis Syndrome ◽  
Geographical Variations ◽  
Human Male ◽  
Testicular Dysgenesis ◽  
Male Reproductive Health

The amount of research into endocrine disruption has exploded over the past decade and a re-evaluation of the state of research in this area is timely. There are debates about whether human male reproductive health is really declining and whether endocrine disrupting chemicals play any role in the perceived decline. Most data currently conclude that there are wide geographical variations in semen quality and in the incidence of testicular cancer, cryptorchidism and hypospadias. This review aims to give a brief overview of the issues surrounding the perceived decline in human male reproductive health and the importance of the hormonal environment for the development of the testis and reproductive tract. The consequences for the male reproductive tract of abnormal androgen levels or action are discussed with reference to environmental anti-androgenic compounds. The in vivo data on several anti-androgenic compounds that have been administered to pregnant rodents during the period of male reproductive tract development are assessed with attention to the effects on the male offspring. Finally, the data on in utero phthalate administration are discussed in detail to illustrate the similarities between the effects of some phthalate esters and the human male reproductive tract disorders which comprise testicular dysgenesis syndrome (TDS).

Carboxylesterase overexpression in the male reproductive tract: a universal safeguarding mechanism?

1999 ◽  
Vol 11 (3) ◽  
pp. 133 ◽  
Author(s):  
A. T. Mikhailov ◽  
M. Torrado
Keyword(s):  
Reproductive Tract ◽  
Expression Patterns ◽  
Cell Lineage ◽  
Environmental Chemicals ◽  
Male Reproductive Tract ◽  
Morphological Organization ◽  
Associated Functions ◽  
And Function ◽  
Hypothetical Explanation

Data on expression patterns of carboxylesterases in the male reproductive tract of different animal groups (i.e. bivalve mollusks, fruitflies and rodents) are summarized to highlight some particularly interesting questions in the context of sperm differentiation, maturation and function. The male reproduc-tive system, in spite of extreme variation in the anatomical/morphological organization in different species, is characterized by similar patterns of male-dependent carboxylesterase overexpression. The phenomenon of conserved carboxylesterase overexpression indicates similar male sex-associated functions of the enzymes. There is possible evidence of carboxylesterase recruitment by male reproductive-tract tissues indi-cating that it could be adaptive for spermatogenesis, sperm maturation and sperm use. Moreover, this idea can be extended to include a sperm cell lineage protection. This issue is discussed in the light of recent data on environmental reproductive xenobiotics that can provide a basis for a hypothetical explanation of car-boxylesterase overexpression in the male reproductive tract. Based on a well-known role of car-boxylesterases in detoxification of environmental chemicals such as organophosphate pesticides, it is proposed that various male genital tract carboxylesterases may be characterized by a similar physiological function to protect the male reproductive system against xenobiotic influences that could provoke its dys-function, thus altering sperm differentiation and maturation.

scholarly journals Location of a membrane-bound carbonic anhydrase isoenzyme (CA IV) in the human male reproductive tract.

1993 ◽  
Vol 41 (5) ◽  
pp. 751-757 ◽  
Author(s):  
S Parkkila ◽  
A K Parkkila ◽  
K Kaunisto ◽  
A Waheed ◽  
W S Sly ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Carbonic Anhydrase ◽  
Reproductive Tract ◽  
Muscle Layer ◽  
Apical Plasma Membrane ◽  
Specific Staining ◽  
Ductus Deferens ◽  
Male Reproductive Tract ◽  
Human Male ◽  
Membrane Bound

We studied the location of a membrane-bound carbonic anhydrase (CA IV) in the human male reproductive tract using a specific antiserum to human CA IV in conjunction with immunoblotting, immunoperoxidase, and immunofluorescence techniques. The microvilli and apical plasma membrane of the epithelial cells and the subepithelial smooth muscle layer of the epididymis, ductus deferens, and ampulla of the ductus deferens showed specific staining for CA IV. The epithelial cells of the prostate and seminal vesicle failed to stain for CA IV, however, whereas the subepithelial smooth muscle layer showed positive staining. No specific staining for CA II was seen in the epithelium of the epididymal duct or the proximal ductus deferens. The presence of CA IV in the epididymis was confirmed by immunoblotting, which revealed 35 KD and 33 KD polypeptides. The results show that the microvilli and the apical plasma membrane of the lining epithelium of the epididymal duct, ductus deferens, and ampulla of the ductus deferens contain the membrane-bound carbonic anhydrase isoenzyme IV. The presence of the enzyme in the epithelium of the epididymis and ductus deferens is probably linked to the acidification of the epididymal fluid that prevents premature sperm activation. Its physiological role in the smooth muscle cells remains to be elucidated.

scholarly journals Zika Virus Trafficking and Interactions in the Human Male Reproductive Tract

Pathogens ◽  
2018 ◽  
Vol 7 (2) ◽  
pp. 51 ◽  
Author(s):  
Lucia Da Silva
Keyword(s):  
Zika Virus ◽  
Reproductive Tract ◽  
Sexual Transmission ◽  
Host Cells ◽  
Future Research ◽  
Mosquito Vector ◽  
Male Reproductive Tract ◽  
Unprotected Sexual Intercourse ◽  
Human Male ◽  
Viral Interactions

Sexual transmission of Zika virus (ZIKV) is a matter of great concern. Infectious viral particles can be shed in semen for as long as six months after infection and can be transferred to male and female sexual partners during unprotected sexual intercourse. The virus can be found inside spermatozoa and could be directly transferred to the oocyte during fertilization. Sexual transmission of ZIKV can contribute to the rise in number of infected individuals in endemic areas as well as in countries where the mosquito vector does not thrive. There is also the possibility, as has been demonstrated in mouse models, that the vaginal deposition of ZIKV particles present in semen could lead to congenital syndrome. In this paper, we review the current literature to understand ZIKV trafficking from the bloodstream to the human male reproductive tract and viral interactions with host cells in interstitial spaces, tubule walls, annexed glands and semen. We hope to highlight gaps to be filled by future research and potential routes for vaccine and antiviral development.

Testicular dysgenesis syndrome and the development and occurrence of male reproductive disorders

2005 ◽  
Vol 207 (2) ◽  
pp. 501-505 ◽  
Author(s):  
H VIRTANEN ◽  
E RAJPERTDEMEYTS ◽  
K MAIN ◽  
N SKAKKEBAEK ◽  
J TOPPARI
Keyword(s):  
Reproductive Disorders ◽  
Testicular Dysgenesis Syndrome ◽  
Testicular Dysgenesis

scholarly journals Phthalate-induced pathology in the foetal testis involves more than decreased testosterone production

Reproduction ◽  
2014 ◽  
Vol 147 (4) ◽  
pp. 435-442 ◽  
Author(s):  
D N Rao Veeramachaneni ◽  
Gary R Klinefelter
Keyword(s):  
Reproductive Tract ◽  
Comprehensive Evaluation ◽  
Male Rats ◽  
Testicular Dysgenesis Syndrome ◽  
Pathway Network ◽  
New Findings ◽  
Testicular Dysgenesis ◽  
And Migration ◽  
And Function ◽  
Rats And Mice

Foetal exposure to phthalates is known to adversely impact male reproductive development and function. Developmental anomalies of reproductive tract have been attributed to impaired testosterone synthesis. However, species differences in the ability to produce testosterone have been noted; e.g., following foetal exposure, abnormal clustering of Leydig cells or decreased production of testosterone that is manifested in rats does not occur in mice or humans. Nonetheless, other facets of testicular dysgenesis occur in both rats and mice as well as in some other species tested. We recently published a comprehensive evaluation of the foetal rat testis proteome, following in utero exposure to diethylhexyl phthalate (DEHP), which revealed changes in individual proteins that are known to be factors in cellular differentiation and migration or related to the capacity of the foetal Leydig cell to produce testosterone and fit a pathway network in which each is regulated directly or indirectly by oestradiol. Plasma oestradiol indeed was found to be elevated approximately twofold in 19-day-old DEHP-exposed foetal male rats. In this brief review, we discuss our new findings vis-à-vis ‘oestrogen hypothesis’ as a cause for testicular dysgenesis syndrome.

scholarly journals Expression of epithelial cadherin in the human male reproductive tract and gametes and evidence of its participation in fertilization

2008 ◽  
Vol 14 (10) ◽  
pp. 561-571 ◽  
Author(s):  
C.I. Marin-Briggiler ◽  
M.F. Veiga ◽  
M.L. Matos ◽  
M.F. Gonzalez Echeverria ◽  
L.I. Furlong ◽  
...  
Keyword(s):  
Reproductive Tract ◽  
Male Reproductive Tract ◽  
Epithelial Cadherin ◽  
Human Male

Expression of dysadherin in the human male reproductive tract and in spermatozoa

2011 ◽  
Vol 96 (3) ◽  
pp. 554-561.e2 ◽  
Author(s):  
Nieves María Gabrielli ◽  
María Florencia Veiga ◽  
María Laura Matos ◽  
Silvina Quintana ◽  
Héctor Chemes ◽  
...  
Keyword(s):  
Reproductive Tract ◽  
Male Reproductive Tract ◽  
Human Male

scholarly journals Deficiency of Reproductive Tract α(1,2)Fucosylated Glycans and Normal Fertility in Mice with Targeted Deletions of the FUT1 or FUT2 α(1,2)Fucosyltransferase Locus

2001 ◽  
Vol 21 (24) ◽  
pp. 8336-8345 ◽  
Author(s):  
Steven E. Domino ◽  
Liang Zhang ◽  
Patrick J. Gillespie ◽  
Thomas L. Saunders ◽  
John B. Lowe
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Reproductive Tract ◽  
Normal Development ◽  
Sperm Maturation ◽  
Male Reproductive Tract ◽  
Uterine Epithelial Cells ◽  
Uterine Epithelial Cell ◽  
Normal Fertility ◽  
Genes Encoding

ABSTRACT The fucose α(1→2) galactose β structure is expressed by uterine epithelial cells in the mouse and has been implicated in blastocyst adhesion events thought to be required for murine implantation. Fucα(1→2)Galβ moieties and cognate fucosyltransferases are also expressed by epithelial cells of the male reproductive tract and have been implicated in sperm maturation events that may contribute to fertilization. To determine directly if Fucα(1→2)Galβ moieties are required for fertility, we have generated strains of mice that are deficient in genes encoding FUT1 and FUT2, a pair of GDP-l-fucose:β(1→4)-d-galactosyl-R2-α-l-fucosyltransferase enzymes (EC 2.4.1.69 ) responsible for Fucα(1→2)Galβ synthesis and expression. FUT1 null mice and FUT2 null mice develop normally and exhibit no gross phenotypic abnormalities. The Fucα(1→2)Galβ epitope is absent from the uterine epithelia of FUT2 null mice and from the epithelia of the epididymis of FUT1 null mice. Fully normal fertility is observed in FUT1 null intercrosses and in FUT2 null intercrosses. These observations indicate that Fucα(1→2)Galβ moieties are not essential to blastocyst-uterine epithelial cell interactions required for implantation and are not required for sperm maturation events that permit fertilization and that neither the FUT loci nor their cognate fucosylated glycans are essential to normal development.

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