Prenatal exposure to the phthalate DEHP modifies the expression of pituitary estrogen receptors and affects reproductive physiology in the adult

Estrogens, acting through Estrogen Receptors (ER) alpha and beta, regulate the pituitary hormonal secretion contributing to the modulation of male sexual function. Estrogenic signaling may be affected by the action of endocrine disruptors such as Di (2-ethylhexyl) phthalate (DEHP), an anthropic prod...

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Autores principales: Pérez, PA, Toledo, J, Luque, ME, Martini, AC, Torres, A, Gutierrez, S
Formato: Artículo revista
Lenguaje:Español
Publicado: Universidad Nacional Córdoba. Facultad de Ciencias Médicas. Secretaria de Ciencia y Tecnología 2019
Materias:
Acceso en línea:https://revistas.unc.edu.ar/index.php/med/article/view/25590
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id I10-R327-article-25590
record_format ojs
institution Universidad Nacional de Córdoba
institution_str I-10
repository_str R-327
container_title_str Revista de la Facultad de Ciencias Médicas de Córdoba
language Español
format Artículo revista
topic estrogen
estrogen receptors
phtalate
pituitary
estrógeno
receptores estrogénicos
ftalato
hipófisis
spellingShingle estrogen
estrogen receptors
phtalate
pituitary
estrógeno
receptores estrogénicos
ftalato
hipófisis
Pérez, PA
Toledo, J
Luque, ME
Martini, AC
Torres, A
Gutierrez, S
Prenatal exposure to the phthalate DEHP modifies the expression of pituitary estrogen receptors and affects reproductive physiology in the adult
topic_facet estrogen
estrogen receptors
phtalate
pituitary
estrógeno
receptores estrogénicos
ftalato
hipófisis
author Pérez, PA
Toledo, J
Luque, ME
Martini, AC
Torres, A
Gutierrez, S
author_facet Pérez, PA
Toledo, J
Luque, ME
Martini, AC
Torres, A
Gutierrez, S
author_sort Pérez, PA
title Prenatal exposure to the phthalate DEHP modifies the expression of pituitary estrogen receptors and affects reproductive physiology in the adult
title_short Prenatal exposure to the phthalate DEHP modifies the expression of pituitary estrogen receptors and affects reproductive physiology in the adult
title_full Prenatal exposure to the phthalate DEHP modifies the expression of pituitary estrogen receptors and affects reproductive physiology in the adult
title_fullStr Prenatal exposure to the phthalate DEHP modifies the expression of pituitary estrogen receptors and affects reproductive physiology in the adult
title_full_unstemmed Prenatal exposure to the phthalate DEHP modifies the expression of pituitary estrogen receptors and affects reproductive physiology in the adult
title_sort prenatal exposure to the phthalate dehp modifies the expression of pituitary estrogen receptors and affects reproductive physiology in the adult
description Estrogens, acting through Estrogen Receptors (ER) alpha and beta, regulate the pituitary hormonal secretion contributing to the modulation of male sexual function. Estrogenic signaling may be affected by the action of endocrine disruptors such as Di (2-ethylhexyl) phthalate (DEHP), an anthropic product used in plastics manufacture, to which we are highly exposed by inhalation, digestive or dermal route. We proposed to analyze the effect of prenatal exposure to DEHP on the pituitary ER levels and its impact on the reproductive physiology. Male Wistar rats prenatally treated with DEHP and maintained until sexual maturity were used. At 3.5 months, the body weight was determined and subsequently the animals were sacrificed to quantify the expression of pituitary ER alpha and beta by flow cytometry, determine testicular weight, anogenital distance, sperm concentration and motility. Statistical analysis: ANOVA-Fisher. Our results showed that prenatal exposure to DEHP decreased the percentage of ERalfa + cells (57.23 ± 0.92% treated vs. 60.19 ± 0.29% controls, P <0.05), together with an increase in ERbeta expression (34.46 ± 3.58% treated vs. 23.13 ± 1.61% controls, P <0.005). The REalfa / beta index was 1.66 ± 0.2 in exposed vs. 2.6 ± 0.09 in controls. A significant decrease in anogenital distance was also observed in prenatally treated animals (1.37 ± 0.06 cm) vs. controls (1.79 ± 0.07 cm)(P <0.05), together with a significant increase in sperm concentration (10.86 x106 ± 1.32 x ml. in treated vs. 6.26 x 106 ± 0.95 x ml. in controls, P <0.05). The percentage of motile sperm did not change significantly. The results also showed a decrease in testicular weight being 2.78 ± 0.03g in exposed vs. 3.49 ± 0.08g in controls (P <0.001), together with a significant increase in body weight of treated animals (356 ± 3.4g) vs. controls (323 ± 1.2g). These results show that prenatal exposure to the phthalate “DEHP” induces changes in the expression of pituitary ERalfa and beta in adulthood and modifies parameters of the reproductive function.
publisher Universidad Nacional Córdoba. Facultad de Ciencias Médicas. Secretaria de Ciencia y Tecnología
publishDate 2019
url https://revistas.unc.edu.ar/index.php/med/article/view/25590
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spelling I10-R327-article-255902024-08-27T18:25:56Z Prenatal exposure to the phthalate DEHP modifies the expression of pituitary estrogen receptors and affects reproductive physiology in the adult La exposición prenatal al ftalato DEHP modifica la expresión de los receptores estrogénicos adenohipofisarios y afecta la fisiología reproductiva en la adultez Pérez, PA Toledo, J Luque, ME Martini, AC Torres, A Gutierrez, S estrogen estrogen receptors phtalate pituitary estrógeno receptores estrogénicos ftalato hipófisis Estrogens, acting through Estrogen Receptors (ER) alpha and beta, regulate the pituitary hormonal secretion contributing to the modulation of male sexual function. Estrogenic signaling may be affected by the action of endocrine disruptors such as Di (2-ethylhexyl) phthalate (DEHP), an anthropic product used in plastics manufacture, to which we are highly exposed by inhalation, digestive or dermal route. We proposed to analyze the effect of prenatal exposure to DEHP on the pituitary ER levels and its impact on the reproductive physiology. Male Wistar rats prenatally treated with DEHP and maintained until sexual maturity were used. At 3.5 months, the body weight was determined and subsequently the animals were sacrificed to quantify the expression of pituitary ER alpha and beta by flow cytometry, determine testicular weight, anogenital distance, sperm concentration and motility. Statistical analysis: ANOVA-Fisher. Our results showed that prenatal exposure to DEHP decreased the percentage of ERalfa + cells (57.23 ± 0.92% treated vs. 60.19 ± 0.29% controls, P <0.05), together with an increase in ERbeta expression (34.46 ± 3.58% treated vs. 23.13 ± 1.61% controls, P <0.005). The REalfa / beta index was 1.66 ± 0.2 in exposed vs. 2.6 ± 0.09 in controls. A significant decrease in anogenital distance was also observed in prenatally treated animals (1.37 ± 0.06 cm) vs. controls (1.79 ± 0.07 cm)(P <0.05), together with a significant increase in sperm concentration (10.86 x106 ± 1.32 x ml. in treated vs. 6.26 x 106 ± 0.95 x ml. in controls, P <0.05). The percentage of motile sperm did not change significantly. The results also showed a decrease in testicular weight being 2.78 ± 0.03g in exposed vs. 3.49 ± 0.08g in controls (P <0.001), together with a significant increase in body weight of treated animals (356 ± 3.4g) vs. controls (323 ± 1.2g). These results show that prenatal exposure to the phthalate “DEHP” induces changes in the expression of pituitary ERalfa and beta in adulthood and modifies parameters of the reproductive function. Los estrógenos, a través de los receptores estrogénicos (RE) alfa y beta, regulan la secreción hormonal adenohipofisaria contribuyendo a la modulación de la función sexual masculina. La señalización estrogénica puede estar afectada por la acción de disruptores endocrinos como Di(2-etilhexil)ftalato (DEHP), producto antrópico utilizado en la fabricación de plásticos, al que estamos altamente expuestos por inhalación, vía digestiva o dérmica. Se propone analizar el efecto de la exposición prenatal al DEHP sobre los niveles de expresión de los RE adenohipofisarios y su impacto sobre la fisiología reproductiva.  Se utilizaron ratas macho Wistar tratadas prenatalmente con DEHP y mantenidas hasta su madurez sexual. A los 3.5 meses, se determinó el peso corporal y posteriormente los animales fueron sacrificados para cuantificar la expresión de RE alfa y beta adenohipofisario por citometría de flujo, determinar peso testicular, distancia ano-genital, concentración y motilidad espermática. Análisis estadístico: ANOVA-Fisher. Nuestros resultados mostraron que la exposición prenatal a DEHP disminuyó el porcentaje de células REalfa+ (57.23 ± 0.92% tratados vs. 60.19 ± 0.29% controles, P<0.05), junto con un incremento en la expresión del REbeta (34.46 ± 3.58% tratados vs. 23.13 ± 1.61% controles, P<0.005). El índice REalfa/beta fue 1.66 ± 0.2 en expuestos vs. 2.6 ± 0.09 en controles. Se observó además una disminución significativa en la distancia ano-genital (1.37 ± 0.06 cm. en animales tratados prenatalmente vs. 1.79 ± 0.07 cm. en controles, P<0.05), junto con un incremento significativo en la concentración espermática (10.86 x106 ± 1.32 x ml. en tratados vs. 6.26 x 106 ± 0.95 x ml. en controles, P<0.05). El porcentaje de espermatozoides móviles no se modificó significativamente. Los resultados mostraron también una disminución del peso testicular siendo de 2.78 ± 0.03g en expuestos vs. 3.49 ± 0.08g en controles (P<0.001), junto con incremento significativo del peso corporal de los animales tratados (356 ± 3.4g) vs. controles (323 ± 1.2g). Estos resultados muestran que la exposición prenatal al ftalato DEHP induce cambios en la expresión de los REalfa y beta adenohipofisarios en la adultez y modifica parámetros de la función reproductiva. Universidad Nacional Córdoba. Facultad de Ciencias Médicas. Secretaria de Ciencia y Tecnología 2019-10-04 info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion application/pdf https://revistas.unc.edu.ar/index.php/med/article/view/25590 Revista de la Facultad de Ciencias Médicas de Córdoba.; 2019: Suplemento JIC XX Revista de la Facultad de Ciencias Médicas de Córdoba; 2019: Suplemento JIC XX Revista da Faculdade de Ciências Médicas de Córdoba; 2019: Suplemento JIC XX 1853-0605 0014-6722 10.31053/1853.0605.v76.nSuplemento spa https://revistas.unc.edu.ar/index.php/med/article/view/25590/27353 Derechos de autor 2019 Universidad Nacional de Córdoba https://creativecommons.org/licenses/by-nc/4.0