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The study investigates how maternal exposure to bisphenol S disrupts thyroid hormone activity and affects testicular development in male offspring.

Maternal Thyroid Disruption: A Probable Key Mechanism of Bisphenol S Induced Testis Development Alteration

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Randomized trial assesses thyroid disruption impact on testicular development in male offspring, suggesting significant developmental impairment.

The study investigates how maternal exposure to bisphenol S disrupts thyroid hormone activity and affects testicular development in male offspring.
Pregnant and lactating Wistar rats were exposed to bisphenol S or a thyroid hormone receptor antagonist.
Testicular development was assessed through histology, testosterone quantification, and expression analysis of SOX9 and CYP17A1.
Evaluations occurred at gestational day 20, postnatal day 21, and postnatal day 35.
BPS exposure reduced body weight and relative testes weight in male offspring at PND21 and PND35.
Decreased serum testosterone levels and seminiferous tubule diameter were observed, along with altered histopathology.
Lower expression of SOX9 and CYP17A1 in Leydig and Sertoli cells indicated impaired testicular development.

Rhouma et al. (2026) studied this question.

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Randomized trial assesses thyroid disruption impact on testicular development in male offspring, suggesting significant developmental impairment.