Respiratory toxicity mechanism of 6PPD and 6PPD-quinone: An integrated study based on network toxicology and molecular docking

The widespread distribution of environmental contaminants poses a significant threat to public health. N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine (6PPD) and its ozone-derivative, 6PPD-quinone (6PPD-Q), are emerging pollutants that propagate through particulate matter and aerosols, exerting detrimental effects on the respiratory system. However, their specific pathogenic mechanisms remain unclear. This study employs integrated network toxicology and molecular docking to elucidate the molecular basis of 6PPD/6PPD-Q-induced respiratory toxicity. Respiratory hazard potential was predicted using ADMETlab 3.0 and ProTox-II. Potential targets were identified through multi-database mining (BindingDB, ChEMBL, SwissTargetPrediction, TargetNet), with disease-associated targets categorized into acute and chronic respiratory damage using GeneCards and OMIM. Intersectional analysis via Venn diagrams, STRING, and Cytoscape revealed compound-specific targets (EGFR for 6PPD; FYN for 6PPD-Q) and five shared targets (NR3C1, MAPK14, RELA, CYCS, JAK2). Enrichment analysis using DAVID indicated significant associations with mitochondrial energy metabolism, oxidative stress, apoptosis and neuroactive ligand-receptor interactions (p < 0.05). Molecular docking and molecular dynamics simulations confirmed that both compounds showed high affinity binding to key toxicity targets (binding energy <-20.92 kJ/mol), and revealed the interaction mode of these two compounds with the key target CYCS. Mechanistically, 6PPD and 6PPD-Q disrupt the mitochondrial electron transport chain, dysregulate apoptotic pathways, and activate NF-κB/JAK-STAT inflammatory cascades, leading to respiratory inflammation. This study establishes a comparative toxicological framework for 6PPD and 6PPD-Q, identifying actionable molecular targets and mechanistic pathways for respiratory toxicity, and highlights the utility of computational toxicology strategies in environmental health risk assessment.

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Journal
Ecotoxicology and Environmental Safety
Published
2025-06-11
DOI
https://doi.org/10.1016/j.ecoenv.2025.118494
Citations
9
Primary Topic
Metabolomics and Mass Spectrometry Studies
Type
article
Field-Weighted Citation Impact
7.25
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article

Respiratory toxicity mechanism of 6PPD and 6PPD-quinone: An integrated study based on network toxicology and molecular docking

Yuan‐Lan Huang, Gang Li, Chang Liu, Dan Li et al.
9 citations
Ecotoxicology and Environmental Safety
Metabolomics and Mass Spectrometry Studies
7.25
article

Respiratory toxicity mechanism of 6PPD and 6PPD-quinone: An integrated study based on network toxicology and molecular docking

Yuan‐Lan Huang, Gang Li, Chang Liu, Dan Li, Qingqiang Xu, Mengying Chen, Weibin Zhai
article en
9 citations

Abstract

The widespread distribution of environmental contaminants poses a significant threat to public health. N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine (6PPD) and its ozone-derivative, 6PPD-quinone (6PPD-Q), are emerging pollutants that propagate through particulate matter and aerosols, exerting detrimental effects on the respiratory system. However, their specific pathogenic mechanisms remain unclear. This study employs integrated network toxicology and molecular docking to elucidate the molecular basis of 6PPD/6PPD-Q-induced respiratory toxicity. Respiratory hazard potential was predicted using ADMETlab 3.0 and ProTox-II. Potential targets were identified through multi-database mining (BindingDB, ChEMBL, SwissTargetPrediction, TargetNet), with disease-associated targets categorized into acute and chronic respiratory damage using GeneCards and OMIM. Intersectional analysis via Venn diagrams, STRING, and Cytoscape revealed compound-specific targets (EGFR for 6PPD; FYN for 6PPD-Q) and five shared targets (NR3C1, MAPK14, RELA, CYCS, JAK2). Enrichment analysis using DAVID indicated significant associations with mitochondrial energy metabolism, oxidative stress, apoptosis and neuroactive ligand-receptor interactions (p < 0.05). Molecular docking and molecular dynamics simulations confirmed that both compounds showed high affinity binding to key toxicity targets (binding energy <-20.92 kJ/mol), and revealed the interaction mode of these two compounds with the key target CYCS. Mechanistically, 6PPD and 6PPD-Q disrupt the mitochondrial electron transport chain, dysregulate apoptotic pathways, and activate NF-κB/JAK-STAT inflammatory cascades, leading to respiratory inflammation. This study establishes a comparative toxicological framework for 6PPD and 6PPD-Q, identifying actionable molecular targets and mechanistic pathways for respiratory toxicity, and highlights the utility of computational toxicology strategies in environmental health risk assessment.

Ecotoxicology and Environmental SafetyVol. 301
Naval Medical Research Command (US), Naval University of Engineering (CN), Naval Aerospace Medical Research Laboratory (US)
Openalex Percentile: Top 3%
Metabolomics and Mass Spectrometry Studies
7.25
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