Abstract
Growing evidence suggests that perfluorinated compounds (PFCs) contribute to reproductive toxicity, with perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) being the most extensively studied. These chemicals are known to lower testosterone levels and compromise the integrity of the blood-testis barrier. However, the specific mechanisms of their reproductive toxicity remain largely unknown due to research limitations. In this study, we utilized network pharmacology to pinpoint the core genes and signaling pathways implicated in the reproductive toxicity caused by PFOA and PFOS. Molecular docking was employed to validate the interactions between these compounds and their targets. Key targets identified include CCL2, CXCR4, RPS27A, RPL5, PSMA7, and PSMC1, which are crucial in mediating reproductive toxicity. These genes are primarily involved in the chemokine signaling pathway, viral protein interactions with cytokines and cytokine receptors, and ribosomal functions. This study underscores the effectiveness of combining network toxicology and molecular docking to analyze the toxicity and molecular mechanisms of mixed environmental pollutants.
Published Version
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