Exposure to the plasticizer DEHP during development and lactation alters the pituitary-testicular axis
Phthalates are additives that give flexibility to polyvinyl chloride (PVC), being Di-2-ethylhexyl phthalate (DEHP) the most widely used due to its low cost and usefulness in the industry. It crosses the placental barrier and interferes with hormonal signaling, acting as an endocrine disruptor, affec...
| Autores principales: | , , , , , , , |
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| Formato: | Artículo revista |
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Universidad Nacional Córdoba. Facultad de Ciencias Médicas. Secretaria de Ciencia y Tecnología
2022
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| Acceso en línea: | https://revistas.unc.edu.ar/index.php/med/article/view/39068 |
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I10-R327-article-39068 |
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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 |
| format |
Artículo revista |
| topic |
dehp pituitary gland gonadotroph testosterone testis dehp hipófisis gonadotropas testosterona testículo |
| spellingShingle |
dehp pituitary gland gonadotroph testosterone testis dehp hipófisis gonadotropas testosterona testículo Perez, PA Toledo , J Ferri, A Díaz, V Cantarelli, V Ponzio, M De Paul, AL Gutierrez, S Exposure to the plasticizer DEHP during development and lactation alters the pituitary-testicular axis |
| topic_facet |
dehp pituitary gland gonadotroph testosterone testis dehp hipófisis gonadotropas testosterona testículo |
| author |
Perez, PA Toledo , J Ferri, A Díaz, V Cantarelli, V Ponzio, M De Paul, AL Gutierrez, S |
| author_facet |
Perez, PA Toledo , J Ferri, A Díaz, V Cantarelli, V Ponzio, M De Paul, AL Gutierrez, S |
| author_sort |
Perez, PA |
| title |
Exposure to the plasticizer DEHP during development and lactation alters the pituitary-testicular axis |
| title_short |
Exposure to the plasticizer DEHP during development and lactation alters the pituitary-testicular axis |
| title_full |
Exposure to the plasticizer DEHP during development and lactation alters the pituitary-testicular axis |
| title_fullStr |
Exposure to the plasticizer DEHP during development and lactation alters the pituitary-testicular axis |
| title_full_unstemmed |
Exposure to the plasticizer DEHP during development and lactation alters the pituitary-testicular axis |
| title_sort |
exposure to the plasticizer dehp during development and lactation alters the pituitary-testicular axis |
| description |
Phthalates are additives that give flexibility to polyvinyl chloride (PVC), being Di-2-ethylhexyl phthalate (DEHP) the most widely used due to its low cost and usefulness in the industry. It crosses the placental barrier and interferes with hormonal signaling, acting as an endocrine disruptor, affecting fetal development. The aim of this study was to analyze the effect of exposure to DEHP during pregnancy and lactation on the pituitary-gonadal axis.
Male Wistar rats exposed during gestation and lactation to DEHP (200 µg/kg/day) or vehicle (corn oil) were sacrificed at 21 days postnatal (DPN, prepubertal period) and 75 DPN (adulthood). Stem blood was obtained for serum testosterone determination. The anterior pituitary glands were processed to determine the percentage of gonadotrophs (immunodetection of βLH) and for the analysis of the proliferative capacity of this endocrine population (Ki-67), by flow cytometry and immunofluorescence. The testis and corpus epididymis were processed for optical morphological and ultrastructural analysis. Statistical analysis ANOVA Tukey (P<0.05) was performed.
Exposure to DEHP significantly reduced serum testosterone concentration by approximately 50% and produced a shortening of the anogenital distance, both in prepuberty and in adulthood, which would be indicative of androgen deficiency during development. In addition, exposure to DEHP decreased the percentage of pituitary gonadotropic cells and inhibited the proliferation of this endocrine cell type. In the testicle, DEHP induced degenerative changes in the seminiferous tubules, with a decrease in the number of layers of the sperm progeny, evidence of hypospermatogenesis, as well as disorganization of the maturational stages. In the epididymis, a significant decrease in the height of the epithelium was observed without alteration of the tubular diameter.
These results suggest that during development, exposure to DEHP disturbs the fetal androgenic environment and alters the pituitary-testicular axis, decreasing the population of gonadotrophs in the pituitary gland and altering testicular function. |
| publisher |
Universidad Nacional Córdoba. Facultad de Ciencias Médicas. Secretaria de Ciencia y Tecnología |
| publishDate |
2022 |
| url |
https://revistas.unc.edu.ar/index.php/med/article/view/39068 |
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2024-09-03T21:04:07Z |
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2024-09-03T21:04:07Z |
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1809210353505009664 |
| spelling |
I10-R327-article-390682024-04-15T16:14:45Z Exposure to the plasticizer DEHP during development and lactation alters the pituitary-testicular axis La exposición al plastificante DEHP durante el desarrollo y la lactancia altera el eje hipofiso-testicular Perez, PA Toledo , J Ferri, A Díaz, V Cantarelli, V Ponzio, M De Paul, AL Gutierrez, S dehp pituitary gland gonadotroph testosterone testis dehp hipófisis gonadotropas testosterona testículo Phthalates are additives that give flexibility to polyvinyl chloride (PVC), being Di-2-ethylhexyl phthalate (DEHP) the most widely used due to its low cost and usefulness in the industry. It crosses the placental barrier and interferes with hormonal signaling, acting as an endocrine disruptor, affecting fetal development. The aim of this study was to analyze the effect of exposure to DEHP during pregnancy and lactation on the pituitary-gonadal axis. Male Wistar rats exposed during gestation and lactation to DEHP (200 µg/kg/day) or vehicle (corn oil) were sacrificed at 21 days postnatal (DPN, prepubertal period) and 75 DPN (adulthood). Stem blood was obtained for serum testosterone determination. The anterior pituitary glands were processed to determine the percentage of gonadotrophs (immunodetection of βLH) and for the analysis of the proliferative capacity of this endocrine population (Ki-67), by flow cytometry and immunofluorescence. The testis and corpus epididymis were processed for optical morphological and ultrastructural analysis. Statistical analysis ANOVA Tukey (P<0.05) was performed. Exposure to DEHP significantly reduced serum testosterone concentration by approximately 50% and produced a shortening of the anogenital distance, both in prepuberty and in adulthood, which would be indicative of androgen deficiency during development. In addition, exposure to DEHP decreased the percentage of pituitary gonadotropic cells and inhibited the proliferation of this endocrine cell type. In the testicle, DEHP induced degenerative changes in the seminiferous tubules, with a decrease in the number of layers of the sperm progeny, evidence of hypospermatogenesis, as well as disorganization of the maturational stages. In the epididymis, a significant decrease in the height of the epithelium was observed without alteration of the tubular diameter. These results suggest that during development, exposure to DEHP disturbs the fetal androgenic environment and alters the pituitary-testicular axis, decreasing the population of gonadotrophs in the pituitary gland and altering testicular function. Los ftalatos son aditivos que otorgan flexibilidad al cloruro de polivinilo, siendo el Di-2-etilhexil ftalato (DEHP) el más utilizado por su bajo costo y utilidad en la industria. Atraviesa la barrera placentaria e interfiere con la señalización hormonal actuando como un disruptor endocrino, afectando el desarrollo fetal. El objetivo de este estudio fue analizar el efecto de la exposición durante la gestación y la lactancia al DEHP sobre el eje hipofiso-gonadal. Se utilizaron ratas Wistar macho expuestas durante la gestación y lactancia a DEHP (200 µg/kg /día) o vehículo (aceite de maíz), los cuales fueron sacrificadas a los 21 días posnatal (DPN, periodo prepuberal) y 75 DPN (adultez), Se obtuvo sangre troncal para la determinación de testosterona sérica. Las glándulas adenohipofisarias fueron procesadas para la determinación del porcentaje de gonadotropas (inmunodetección de βLH) y para el análisis de la capacidad proliferativa de esta población endocrina (Ki-67), por citometría de flujo e inmunofluorescencia. Los testículos y cuerpo de epidídimo fueron procesados para el análisis morfológico óptico y ultraestructural. Se realizó análisis estadístico ANOVA Tukey (P<0.05). La exposición a DEHP redujo significativamente la concentración de testosterona sérica en aproximadamente un 50% y produjo un acortamiento de la distancia ano-genital, tanto en la prepubertad como en la adultez, lo cual sería indicativo de deficiencia de andrógenos durante el desarrollo. Además, la exposición a DEHP disminuyó el porcentaje de células gonadotropas en adenohipófisis e inhibió la proliferación de este tipo celular endocrino. En testículo DEHP indujo cambios degenerativos de los túbulos seminíferos, observándose disminución del número de capas de la progenie espermática, evidencia de hipoespermatogénesis, así como desorganización de los estadios madurativos. En epidídimo se observó una disminución significativa de la altura del epitelio sin alteración del diámetro tubular. Estos resultados sugieren que la exposición a DEHP durante el desarrollo perturba el ambiente androgénico fetal y altera el eje hipofiso-testicular, disminuyendo la población de gonadotropas en adenohipófisis y alterando la función testicular. Universidad Nacional Córdoba. Facultad de Ciencias Médicas. Secretaria de Ciencia y Tecnología 2022-10-26 info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion texto texto texto https://revistas.unc.edu.ar/index.php/med/article/view/39068 Revista de la Facultad de Ciencias Médicas de Córdoba.; Vol. 79 No. Suplemento JIC XXIII (2022): Suplemento JIC XXIII Revista de la Facultad de Ciencias Médicas de Córdoba; Vol. 79 Núm. Suplemento JIC XXIII (2022): Suplemento JIC XXIII Revista da Faculdade de Ciências Médicas de Córdoba; v. 79 n. Suplemento JIC XXIII (2022): Suplemento JIC XXIII 1853-0605 0014-6722 http://creativecommons.org/licenses/by-nc/4.0 |