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Transcriptomic analysis of mouse testes with disordered spermatogenesis induced by high-dose BPA exposure during
Ke Hu1,2, Qinran Zhu1, Yifan Xu1
1School of Life Science, Bengbu Medical University, Bengbu, 233030, Anhui Province, China.
Bisphenol A (BPA) exposure during puberty impairs mouse spermatogenesis, altering testicular gene expression. High doses significantly changed numerous genes, including those in extracellular matrix interactions, impacting sperm health.
Area of Science:
- Reproductive Biology
- Endocrinology
- Toxicology
Background:
- Bisphenol A (BPA) is an endocrine disruptor with known adverse effects on reproductive health.
- Limited information exists regarding BPA's impact on testicular mRNA expression profiles.
Purpose of the Study:
- To investigate the effects of BPA exposure on the transcriptome of mouse testes.
- To identify gene expression changes associated with BPA-induced spermatogenesis impairment.
Main Methods:
- Pubertal mice were administered varying doses of BPA (30 and 300 mg/kg/d) via intragastric gavage for 50 days.
- Transcriptomic analysis (RNA sequencing) was performed on testicular tissue.
- Quantitative real-time PCR (RT-qPCR) was used to validate key gene expression changes.
Main Results:
- BPA exposure for 50 days caused significant, dose-dependent sperm damage.
- Transcriptomic analysis revealed significant alterations in gene expression, with thousands of genes upregulated and downregulated at higher BPA doses.
- The extracellular matrix (ECM)-receptor interaction pathway was identified as significantly affected.
- RT-qPCR confirmed differential expression of specific genes (Plekha4, Cd24a, Fos, Srd5a1, Nrg3, Abca4).
Conclusions:
- Pubertal exposure to high-dose BPA significantly impairs spermatogenesis in mice.
- BPA exposure induces widespread changes in testicular gene expression, affecting pathways like ECM-receptor interaction.
- These findings highlight the potential risks of BPA on male reproductive health and provide insights into molecular mechanisms.
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