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A Microplate Assay to Assess Chemical Effects on RBL-2H3 Mast Cell Degranulation: Effects of Triclosan without Use of an Organic Solvent
Published on: November 1, 2013
Exploring potential toxicological pathways of triclosan in human ovarian dysfunction via integrated network
Yu Zhang1, Shaolong Cheng2, Mingquan Huang3
1Department of Ultrasound, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Abstract:
Triclosan (TCS), a compound ubiquitous in personal care products, is now a prevalent environmental contaminant across various ecosystems and has been detected in human tissue samples. Despite its prevalence and strong association with female infertility, the mechanisms by which TCS induces ovarian toxicity have not been thoroughly studied. This study employed an integrated approach combining network toxicology, molecular docking, transcriptomics, and cell experiments to systematically investigate the molecular mechanisms linking TCS to two core ovarian dysfunction diseases: polycystic ovary syndrome (PCOS) and premature ovarian insufficiency (POI). The physicochemical properties and multi-organ toxicity of TCS were predicted using ADMETlab 3.0 and SwissADME. Following the retrieval of TCS, PCOS, and POI-associated targets from public databases, a PPI network was built to pinpoint central hubs. Subsequently, GO and KEGG enrichment analyses were conducted to delineate implicated biological pathways. Molecular docking was conducted to evaluate the binding affinity of TCS to core proteins. Transcriptomic analysis was performed on the ovarian granulosa cell line KGN exposed to 10 μM TCS, a concentration close to human exposure levels. Cell biology experiments were further employed to validate the findings. The network toxicology results indicated that TCS induces ovarian toxicity primarily by promoting apoptosis and triggering inflammatory responses. Key targets identified included AKT1, EGFR, TNF, IL6, and CASP3, which exhibited strong binding affinities, suggesting direct interactions. Transcriptomic analyses further confirmed disruptions in cytokine receptor binding and apoptosis pathways. Cell experiments confirmed that TCS exposure significantly promotes apoptosis and increases the production of inflammatory cytokines in two types of ovarian granulosa cell lines, SVOG and KGN. Overall, this study provides a conceptual framework for TCS-induced ovarian dysfunction and offers new insights for future research on the mechanisms underlying the ovarian toxicity of TCS.
Insights
Triclosan (TCS) exposure promotes ovarian toxicity by increasing apoptosis and inflammation, contributing to infertility. This study reveals key molecular targets involved in polycystic ovary syndrome (PCOS) and premature ovarian insufficiency (POI).
Area of Science:
- Environmental Toxicology
- Reproductive Biology
- Computational Toxicology
Background:
- Triclosan (TCS), a common personal care product ingredient, is a widespread environmental contaminant.
- TCS is linked to female infertility, but its ovarian toxicity mechanisms are poorly understood.
- Polycystic ovary syndrome (PCOS) and premature ovarian insufficiency (POI) are major causes of female reproductive dysfunction.
Purpose of the Study:
- To elucidate the molecular mechanisms underlying TCS-induced ovarian toxicity.
- To investigate the link between TCS exposure and the pathogenesis of PCOS and POI.
- To identify key molecular targets and pathways affected by TCS in ovarian cells.
Main Methods:
- Integrated network toxicology, molecular docking, transcriptomics, and cell experiments.
- ADMET and SwissADME for physicochemical and toxicity prediction.
- Protein-protein interaction network construction, GO and KEGG enrichment analyses.
- Molecular docking to assess TCS-protein binding affinity.
- Transcriptomic analysis of KGN cells exposed to TCS.
- Validation using SVOG and KGN cell lines.
Main Results:
- TCS induces ovarian toxicity primarily through apoptosis promotion and inflammatory responses.
- Key identified targets (AKT1, EGFR, TNF, IL6, CASP3) showed strong binding affinities to TCS.
- Transcriptomic analysis revealed disruptions in cytokine receptor binding and apoptosis pathways.
- Cell experiments confirmed TCS-induced apoptosis and increased inflammatory cytokine production.
Conclusions:
- This study provides a mechanistic framework for TCS-induced ovarian dysfunction.
- TCS exposure poses a significant risk to ovarian health and female fertility.
- Identified molecular targets offer potential avenues for therapeutic interventions.
