Transcriptomic analysis of mouse testes with disordered spermatogenesis induced by high-dose BPA exposure during...

Bisphenol A (BPA) can simulate estrogen, disrupt the endocrine system, affect the development of the nervous and immune systems, and cause fertility problems, precocious puberty, and even lead to various hormone-related cancers. However, little is known about the mRNA expression profile in testes exposed to BPA.

This study focuses on the transcriptome of mouse testes with impaired spermatogenesis induced by BPA exposure during puberty. Twenty-one-day-old mice were treated with 30 and 300 mg/kg/d BPA by intragastric administration for a specific number of days prior to transcriptomic analysis. No significant damage to spermatogenesis was observed after intragastric administration with 30 and 300 mg/kg/d BPA for 10 and 30 days. However, significant sperm damage was observed after 50 days of treatment with both doses, showing a concentration-dependent effect. Transcriptomic analysis of testes from mice treated for 50 days revealed 126 significantly upregulated and 32 significantly downregulated genes in 30 mg/kg/d BPA-treated testes, and 775 significantly upregulated and 695 significantly downregulated genes in 300 mg/kg/d BPA-treated testes. The extracellular matrix (ECM)-receptor interaction signaling pathway was involved in regulating the spermatogenesis of BPA-treated testes. RT-qPCR confirmed that BPA (30 and 300 mg/kg/d) significantly increased testicular mRNA levels of Plekha4, Cd24a, and Fos, and decreased those of Srd5a1, Nrg3, and Abca4.

Transcriptomic analysis of mouse testes with impaired spermatogenesis induced by high-dose BPA exposure during puberty, revealing significantly upregulated and downregulated genes.