Chronic environmental level exposure to perfluorooctane sulfonate overshadows graphene oxide to induce apoptosis through activation of the ROS-p53-caspase pathway in marine medaka Oryzias melastigma.

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  • Additional Information
    • Source:
      Publisher: Elsevier Science Ltd Country of Publication: England NLM ID: 0320657 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1879-1298 (Electronic) Linking ISSN: 00456535 NLM ISO Abbreviation: Chemosphere Subsets: MEDLINE
    • Publication Information:
      Publication: Oxford : Elsevier Science Ltd
      Original Publication: Oxford, New York, : Pergamon Press.
    • Subject Terms:
      Graphite*/toxicity ; Apoptosis*/drug effects ; Fluorocarbons*/toxicity ; Alkanesulfonic Acids*/toxicity ; Reactive Oxygen Species*/metabolism ; Water Pollutants, Chemical*/toxicity ; Oryzias*/metabolism ; Oryzias*/physiology ; Caspases*/metabolism ; Tumor Suppressor Protein p53*/metabolism; Animals ; Signal Transduction/drug effects ; Molecular Docking Simulation ; Environmental Exposure/adverse effects
    • Abstract:
      The widespread occurrence of perfluorooctane sulfonate (PFOS) and the mass production and application of graphene oxide (GO) lead to their inevitable release and interaction in the environment, which may enhance associated toxic impacts on aquatic organisms. This study elucidates the induction of apoptosis by 60-day chronic single and mixture exposures to environmentally relevant levels of PFOS (0.5 μg/L and 5 μg/L) and GO (1 mg/L) in adult marine medaka Oryzias melastigma. Results showed a significant increase (p < 0.05) in reactive oxygen species (ROS) levels, the apoptotic positive rate in livers, and activities of caspases 3, 8, and 9 in all treated groups compared to the control. PFOS individual and PFOS-GO combined exposures significantly impacted fish growth, upregulated expressions of six apoptosis-related genes including p53, apaf1, il1b, tnfa, bcl2l1, bax, as well as enriched cell cycle and p53 signaling pathways (transcriptomic analysis) related to apoptosis compared to control group. Besides higher ROS production, GO also had a higher binding affinity to proteins than PFOS, especially to caspase 8 as revealed by molecular docking. Overall, PFOS induced ROS-p53-caspase apoptosis pathway through multi-gene regulation during single or mixture exposure, while GO single exposure induced apoptosis through tissue damage and ROS-caspase pathway activation and direct docking with caspase 8 to activate the caspase cascade. Under co-exposure, the PFOS-induced apoptotic pathway overshadowed the GO-induced pathway, due to competition for limited active sites on caspases. These findings will contribute to a better understanding of the apoptosis mechanism and ecological risks of nanomaterials and per- and polyfluoroalkyl substances in marine ecosystems.
      Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
      (Copyright © 2024 Elsevier Ltd. All rights reserved.)
    • Contributed Indexing:
      Keywords: Apoptosis; Graphene oxide (GO); Marine medaka; Perfluorooctane sulfonate (PFOS); Transcriptome analysis
    • Accession Number:
      7782-42-5 (Graphite)
      9H2MAI21CL (perfluorooctane sulfonic acid)
      0 (Fluorocarbons)
      0 (Alkanesulfonic Acids)
      0 (Reactive Oxygen Species)
      0 (Water Pollutants, Chemical)
      0 (graphene oxide)
      EC 3.4.22.- (Caspases)
      0 (Tumor Suppressor Protein p53)
    • Publication Date:
      Date Created: 20240921 Date Completed: 20241011 Latest Revision: 20241011
    • Publication Date:
      20241011
    • Accession Number:
      10.1016/j.chemosphere.2024.143374
    • Accession Number:
      39306112