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Published on: April 26, 2018
Maternal Thyroid Disruption: A Probable Key Mechanism of Bisphenol S Induced Testis Development Alteration
Mariem Ben Rhouma1, Lina Chouchene1, Massimo Venditti2
1Laboratory of Genetics, Biodiversity and Bio-Resources Valorization, Higher Institute of Biotechnology of Monastir, University of Monastir, Monastir, Tunisia.
Maternal exposure to Bisphenol S (BPS) disrupts male offspring testicular development by blocking thyroid hormone receptors. This endocrine disruption impacts key developmental markers and gene expression, similar to thyroid hormone receptor antagonists.
Area of Science:
- Endocrinology
- Reproductive Toxicology
- Environmental Health
Background:
- Bisphenol S (BPS) is a common bisphenol A substitute found in consumer products.
- Emerging evidence indicates BPS acts as an endocrine disruptor, potentially affecting thyroid hormone (TH) regulation and testicular function.
- Understanding the impact of BPS on testicular development is crucial due to its widespread use.
Purpose of the Study:
- To assess the impact of maternal Bisphenol S (BPS) exposure on testicular development in male offspring.
- To investigate the role of thyroid hormone receptor (THR) antagonism in BPS-induced testicular effects.
Main Methods:
- Pregnant and lactating Wistar rats were exposed to BPS or a THR antagonist (AT 1-850).
- Testicular development was assessed at gestational day 20, postnatal day 21, and postnatal day 35.
- Evaluations included histology, testosterone levels, and SOX9/CYP17A1 expression in Leydig and Sertoli cells.
Main Results:
- BPS exposure reduced offspring body weight, relative testes weight, anogenital distance, serum testosterone, and seminiferous tubule diameter.
- Histopathological alterations and impaired testicular development were observed in BPS-exposed offspring.
- BPS exposure decreased SOX9 and CYP17A1 expression, mirroring effects seen with the THR antagonist AT 1-850.
Conclusions:
- Maternal BPS exposure significantly disrupts testicular development in male offspring.
- BPS exerts its effects by blocking nuclear thyroid hormone receptors (THRs) during fetal and postnatal development.
- The findings highlight BPS as a concerning endocrine disruptor impacting reproductive health.
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