DEHP Phthalate Induces a Reversible Inhibitory Effect on Testicular Expression of ERα
The di(2-ethylhexyl) phthalate (DEHP) is a ubiquitous environmental contaminant that acts as an endocrine disruptor. It enters the body through ingestion, inhalation, or dermal contact, and crosses the placental barrier, affecting fetal development. The aim of this study was to analyze whether...
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| Autores principales: | , , , , , |
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| Formato: | Artículo revista |
| Lenguaje: | Español |
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Universidad Nacional Córdoba. Facultad de Ciencias Médicas. Secretaria de Ciencia y Tecnología
2023
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| Acceso en línea: | https://revistas.unc.edu.ar/index.php/med/article/view/42665 |
| Aporte de: |
| Sumario: | The di(2-ethylhexyl) phthalate (DEHP) is a ubiquitous environmental contaminant that acts as an endocrine disruptor. It enters the body through ingestion, inhalation, or dermal contact, and crosses the placental barrier, affecting fetal development. The aim of this study was to analyze whether DEHP exposure during development affects the expression of estrogen receptor alpha (ERα) in the testes using a murine model.
Male Wistar rat pups were exposed to 200 µg/kg/day of DEHP (n=15) during gestation and lactation (equivalent to habitual environmental exposure), while control animals were exposed to the vehicle (corn oil) (n=15). Pups were sacrificed either at 21 days (prepubertal period) or 75 postnatal days (adulthood). Body weight, gonadal weight, anogenital distance, and the expression and cellular localization of ERα in the testes were determined using immunohistochemistry and flow cytometry, in addition to a histopathological analysis of the testes by light microscopy. Statistical analysis: ANOVA-Tukey.
Both prepubertal and adult animals exposed to DEHP showed significant changes in general body parameters compared to controls, including increased body weight, decreased gonadal weight, and shortened anogenital distance. Quantification of testicular cells expressing ERα showed that DEHP exposure induced a significant decrease in the number of ERα+ cells in prepubertal animals. However, no changes in the expression of this receptor were observed in adult animals. Both exposed and control animals exhibited ERα in the nuclear compartment of germ cells, peritubular cells, and Leydig cells, with no immunostaining in Sertoli cells. Histopathological analysis of testicular tissue revealed morphological changes in the seminiferous tubules of adult animals, indicative of hypo-spermatogenesis and a significant decrease in epithelial height in the epididymal body.
These results demonstrate that DEHP exposure during gestation and lactation affects gonadal development, leading to morphological alterations in the testes and epididymis of exposed offspring in adulthood, with reversible changes in ERα expression patterns that normalize when phthalate exposure ceases.
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