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Published on: March 1, 2019
Screening 16 bisphenol analogues in asthenospermia: BPM-CDK1 axis identified by computational and In Vitro validation
Siqing Hu1, Ling Ding1, Yiwei Zhao1
1Key Laboratory of Human Genetics and Environmental Medicine, School of Public Health, Xuzhou Medical University, Xuzhou 221004, China.
Reproductive Toxicology (Elmsford, N.Y.)
|May 28, 2026
Summary
Bisphenol analogues (BPs) like BPM disrupt sperm motility by downregulating CDK1 expression, contributing to asthenospermia pathogenesis. This study identifies BPs as a risk factor for male reproductive health issues.
Area of Science:
- Environmental Toxicology
- Reproductive Biology
- Computational Toxicology
Background:
- Bisphenol A (BPA) and its analogues (BPs) are widespread industrial chemicals with documented endocrine-disrupting and reproductive toxicity.
- The use of "BPA-free" alternatives raises concerns about their comparable health risks, particularly in male reproductive health.
Purpose of the Study:
- To systematically evaluate the pathogenic mechanisms of 16 bisphenol congeners in asthenospermia using a network toxicology framework.
- To identify key bisphenol compounds and their molecular targets involved in sperm motility disorders.
Main Methods:
- Integrated screening of disease-target associations and network analysis to identify lead bisphenol compounds.
- Protein-Protein Interaction (PPI) networks, LASSO, Random Forest, Logistic Regression, Naive Bayes, SVM, and XGBoost for target prioritization.
- Molecular docking and dynamics simulations to assess binding affinity and complex stability; in vitro experiments to validate findings.
Main Results:
- Five lead compounds (BPA, BPS, BPB, BPP, BPM) showed significant correlation with sperm motility disorders.
- CDK1 was identified as a core target with high binding affinity to BPs, particularly BPM.
- BPM exposure impaired cell migration and downregulated CDK1 expression in vitro, suggesting a role in asthenospermia pathogenesis.
Conclusions:
- Bisphenol analogues contribute to asthenospermia by disrupting cell proliferation and cycle regulation.
- The BPM-mediated suppression of the CDK1 axis is a key mechanism underlying BP-induced reproductive toxicity.
- Further investigation into BPs' impact on male reproductive health is warranted.
