Molecular biology reports · 2026
Transcriptomic analysis of mouse testes with disordered spermatogenesis induced by high-dose BPA exposure during puberty.
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Hu Ke, Zhu Qinran, Xu Yifan, Han Xuefeng, Pei Zhihan, Liang Meng, Liu Lei
Аннотация
BACKGROUND: 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.
METHODS AND RESULTS: 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.
CONCLUSIONS: Transcriptomic analysis of mouse testes with impaired spermatogenesis induced by high-dose BPA exposure during puberty, revealing significantly upregulated and downregulated genes.
METHODS AND RESULTS: 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.
CONCLUSIONS: Transcriptomic analysis of mouse testes with impaired spermatogenesis induced by high-dose BPA exposure during puberty, revealing significantly upregulated and downregulated genes.