Perfluoroalkyl sulfonate induces cardiomyocyte apoptosis via endoplasmic reticulum stress activation and autophagy flux inhibition.

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  • Additional Information
    • Source:
      Publisher: Elsevier Country of Publication: Netherlands NLM ID: 0330500 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1879-1026 (Electronic) Linking ISSN: 00489697 NLM ISO Abbreviation: Sci Total Environ Subsets: MEDLINE
    • Publication Information:
      Original Publication: Amsterdam, Elsevier.
    • Subject Terms:
      Endoplasmic Reticulum Stress*/drug effects ; Myocytes, Cardiac*/drug effects ; Apoptosis*/drug effects ; Autophagy*/drug effects ; Fluorocarbons*/toxicity ; Alkanesulfonic Acids*/toxicity; Humans ; Cell Line ; Environmental Pollutants/toxicity
    • Abstract:
      Perfluoroalkyl sulfonate (PFOS) is a commonly used chemical compound that often found in materials such as waterproofing agents, food packaging, and fire retardants. Known for its stability and persistence in the environment, PFOS can enter the human body through various pathways, including water and the food chain, raising concerns about its potential harm to human health. Previous studies have suggested a cardiac toxicity of PFOS, but the specific cellular mechanisms remained unclear. Here, by using AC16 cardiomyocyte as a model to investigate the molecular mechanisms potential the cardiac toxicity of PFOS. Our findings revealed that PFOS exposure reduced cell viability and induces apoptosis in human cardiomyocyte. Proteomic analysis and molecular biological techniques showed that the Endoplasmic Reticulum (ER) stress-related pathways were activated, while the cellular autophagy flux was inhibited in PFOS-exposed cells. Subsequently, we employed strategies such as autophagy activation and ER stress inhibition to alleviate the PFOS-induced apoptosis in AC16 cells. These results collectively suggest that PFOS-induced ER stress activation and autophagy flux inhibition contribute to cardiomyocyte apoptosis, providing new insights into the mechanisms of PFOS-induced cardiomyocyte toxicity.
      Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests to be declared.
      (Copyright © 2024 Elsevier B.V. All rights reserved.)
    • Contributed Indexing:
      Keywords: Autophagy; Cardiomyocyte; Cardiotoxicity; ER stress; Perfluoroalkyl sulfonate
    • Accession Number:
      0 (Fluorocarbons)
      0 (Alkanesulfonic Acids)
      9H2MAI21CL (perfluorooctane sulfonic acid)
      0 (Environmental Pollutants)
    • Publication Date:
      Date Created: 20240422 Date Completed: 20240514 Latest Revision: 20240514
    • Publication Date:
      20240514
    • Accession Number:
      10.1016/j.scitotenv.2024.172582
    • Accession Number:
      38649052