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Cellular origins of testicular dysgenesis in rats exposed in utero to di(n-butyl) phthalate

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Cellular origins of testicular dysgenesis in rats exposed in utero to di(n-butyl) phthalate. / Mahood, I Kim; McKinnell, Chris; Walker, Marion; Hallmark, Nina; Scott, Hayley; Fisher, Jane S; Rivas, Ana; Hartung, Stefan; Ivell, Richard; Mason, J Ian; Sharpe, Richard M.

in: INT J ANDROL, Jahrgang 29, Nr. 1, 01.02.2006, S. 148-54; discussion 181-5.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Mahood, IK, McKinnell, C, Walker, M, Hallmark, N, Scott, H, Fisher, JS, Rivas, A, Hartung, S, Ivell, R, Mason, JI & Sharpe, RM 2006, 'Cellular origins of testicular dysgenesis in rats exposed in utero to di(n-butyl) phthalate', INT J ANDROL, Jg. 29, Nr. 1, S. 148-54; discussion 181-5. https://doi.org/10.1111/j.1365-2605.2005.00574.x

APA

Mahood, I. K., McKinnell, C., Walker, M., Hallmark, N., Scott, H., Fisher, J. S., Rivas, A., Hartung, S., Ivell, R., Mason, J. I., & Sharpe, R. M. (2006). Cellular origins of testicular dysgenesis in rats exposed in utero to di(n-butyl) phthalate. INT J ANDROL, 29(1), 148-54; discussion 181-5. https://doi.org/10.1111/j.1365-2605.2005.00574.x

Vancouver

Mahood IK, McKinnell C, Walker M, Hallmark N, Scott H, Fisher JS et al. Cellular origins of testicular dysgenesis in rats exposed in utero to di(n-butyl) phthalate. INT J ANDROL. 2006 Feb 1;29(1):148-54; discussion 181-5. https://doi.org/10.1111/j.1365-2605.2005.00574.x

Bibtex

@article{0a5af8628d4549059abc83a8d7315757,
title = "Cellular origins of testicular dysgenesis in rats exposed in utero to di(n-butyl) phthalate",
abstract = "Foetal exposure of male rats to di(n-butyl) phthalate (DBP) induces testicular changes similar to testicular dysgenesis syndrome in humans, including the formation of focal 'dysgenetic areas' within post-natal testes, surrounded by otherwise normal tubules exhibiting complete spermatogenesis. We hypothesize that these dysgenetic areas form when Sertoli (and other) cells are 'trapped' during the abnormal formation of large Leydig cell (LC) clusters in foetal life and by post-natal day (d) 4 these groups of intermingled cells attempt to form seminiferous tubules. It is likely that the malformed tubules resulting correspond to the dysgenetic areas evident in later life. This also provides a plausible explanation for the occurrence of LCs within seminiferous cords/tubules in or bordering the dysgenetic areas. In our previous studies intratubular LCs (ITLCs) were identified by immunostaining for 3beta-hydroxysteroid dehydrogenase (3beta-HSD), the definitive LC cytoplasmic marker. However, the possibility remained that the 'presumptive' ITLCs were in fact Sertoli cells that had aberrantly gained the ability to express 3beta-HSD. Therefore, the aim of the present study was to fully characterize the ITLCs induced by in utero DBP exposure in d25 rats using a number of LC- (3beta-HSD, P450 side-chain cleavage enzyme, insulin-like factor 3, oestrogen receptor alpha) and Sertoli cell- (vimentin, Wilm's tumour-1) specific markers. Our results show that ITLCs express all four LC-specific markers but do not express either of the Sertoli cell markers. It is therefore concluded that the ITLCs are bona fide LCs that are abnormally located within the seminiferous tubules of DBP-exposed rats in post-natal life.",
keywords = "Androgen Antagonists, Animals, Dibutyl Phthalate, Disease Models, Animal, Female, Humans, Leydig Cells, Male, Maternal Exposure, Pregnancy, Prenatal Exposure Delayed Effects, Rats, Rats, Wistar, Sertoli Cells, Testis",
author = "Mahood, {I Kim} and Chris McKinnell and Marion Walker and Nina Hallmark and Hayley Scott and Fisher, {Jane S} and Ana Rivas and Stefan Hartung and Richard Ivell and Mason, {J Ian} and Sharpe, {Richard M}",
year = "2006",
month = feb,
day = "1",
doi = "10.1111/j.1365-2605.2005.00574.x",
language = "English",
volume = "29",
pages = "148--54; discussion 181--5",
number = "1",

}

RIS

TY - JOUR

T1 - Cellular origins of testicular dysgenesis in rats exposed in utero to di(n-butyl) phthalate

AU - Mahood, I Kim

AU - McKinnell, Chris

AU - Walker, Marion

AU - Hallmark, Nina

AU - Scott, Hayley

AU - Fisher, Jane S

AU - Rivas, Ana

AU - Hartung, Stefan

AU - Ivell, Richard

AU - Mason, J Ian

AU - Sharpe, Richard M

PY - 2006/2/1

Y1 - 2006/2/1

N2 - Foetal exposure of male rats to di(n-butyl) phthalate (DBP) induces testicular changes similar to testicular dysgenesis syndrome in humans, including the formation of focal 'dysgenetic areas' within post-natal testes, surrounded by otherwise normal tubules exhibiting complete spermatogenesis. We hypothesize that these dysgenetic areas form when Sertoli (and other) cells are 'trapped' during the abnormal formation of large Leydig cell (LC) clusters in foetal life and by post-natal day (d) 4 these groups of intermingled cells attempt to form seminiferous tubules. It is likely that the malformed tubules resulting correspond to the dysgenetic areas evident in later life. This also provides a plausible explanation for the occurrence of LCs within seminiferous cords/tubules in or bordering the dysgenetic areas. In our previous studies intratubular LCs (ITLCs) were identified by immunostaining for 3beta-hydroxysteroid dehydrogenase (3beta-HSD), the definitive LC cytoplasmic marker. However, the possibility remained that the 'presumptive' ITLCs were in fact Sertoli cells that had aberrantly gained the ability to express 3beta-HSD. Therefore, the aim of the present study was to fully characterize the ITLCs induced by in utero DBP exposure in d25 rats using a number of LC- (3beta-HSD, P450 side-chain cleavage enzyme, insulin-like factor 3, oestrogen receptor alpha) and Sertoli cell- (vimentin, Wilm's tumour-1) specific markers. Our results show that ITLCs express all four LC-specific markers but do not express either of the Sertoli cell markers. It is therefore concluded that the ITLCs are bona fide LCs that are abnormally located within the seminiferous tubules of DBP-exposed rats in post-natal life.

AB - Foetal exposure of male rats to di(n-butyl) phthalate (DBP) induces testicular changes similar to testicular dysgenesis syndrome in humans, including the formation of focal 'dysgenetic areas' within post-natal testes, surrounded by otherwise normal tubules exhibiting complete spermatogenesis. We hypothesize that these dysgenetic areas form when Sertoli (and other) cells are 'trapped' during the abnormal formation of large Leydig cell (LC) clusters in foetal life and by post-natal day (d) 4 these groups of intermingled cells attempt to form seminiferous tubules. It is likely that the malformed tubules resulting correspond to the dysgenetic areas evident in later life. This also provides a plausible explanation for the occurrence of LCs within seminiferous cords/tubules in or bordering the dysgenetic areas. In our previous studies intratubular LCs (ITLCs) were identified by immunostaining for 3beta-hydroxysteroid dehydrogenase (3beta-HSD), the definitive LC cytoplasmic marker. However, the possibility remained that the 'presumptive' ITLCs were in fact Sertoli cells that had aberrantly gained the ability to express 3beta-HSD. Therefore, the aim of the present study was to fully characterize the ITLCs induced by in utero DBP exposure in d25 rats using a number of LC- (3beta-HSD, P450 side-chain cleavage enzyme, insulin-like factor 3, oestrogen receptor alpha) and Sertoli cell- (vimentin, Wilm's tumour-1) specific markers. Our results show that ITLCs express all four LC-specific markers but do not express either of the Sertoli cell markers. It is therefore concluded that the ITLCs are bona fide LCs that are abnormally located within the seminiferous tubules of DBP-exposed rats in post-natal life.

KW - Androgen Antagonists

KW - Animals

KW - Dibutyl Phthalate

KW - Disease Models, Animal

KW - Female

KW - Humans

KW - Leydig Cells

KW - Male

KW - Maternal Exposure

KW - Pregnancy

KW - Prenatal Exposure Delayed Effects

KW - Rats

KW - Rats, Wistar

KW - Sertoli Cells

KW - Testis

U2 - 10.1111/j.1365-2605.2005.00574.x

DO - 10.1111/j.1365-2605.2005.00574.x

M3 - SCORING: Journal article

C2 - 16466534

VL - 29

SP - 148-54; discussion 181-5

IS - 1

ER -