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Updated: May 26, 2026

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Histopathology and Transcriptomics in Male Zebrafish Livers from a PFOS Multi-Generational Exposure Informs Adverse

J Erik Mylroie1,2, Kurt A Gust1, Chad Blanksma3

  • 1US Army, Engineer Research and Development Center, Environmental Laboratory 3909 Halls Ferry Rd., Vicksburg, MS.

Environmental Toxicology and Chemistry
|May 24, 2026
PubMed
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Perfluorooctanesulfonic acid (PFOS) exposure causes liver damage and disrupts lipid metabolism in zebrafish across two generations. These findings highlight PFOS as a risk factor for liver steatosis, impacting both parental and offspring health.

Area of Science:

  • Environmental Toxicology
  • Molecular Biology
  • Zebrafish Models

Background:

  • Poly- and perfluoroalkyl substances (PFAS) are persistent environmental contaminants.
  • PFAS, such as PFOS, accumulate in vertebrate liver tissue, potentially causing hepatotoxicity.
  • Zebrafish are a valuable model organism for studying toxicological effects due to their genetic similarity to humans and rapid development.

Purpose of the Study:

  • To investigate the tissue-level and molecular effects of PFOS exposure on zebrafish livers across two generations.
  • To characterize histopathological changes and transcriptomic alterations induced by PFOS.
  • To develop an adverse outcome pathway (AOP) linking PFOS exposure to liver steatosis.

Main Methods:

  • Male zebrafish (Danio rerio) were exposed to varying concentrations of PFOS (0-100 µg/L) for 180 days across parental (P) and first filial (F1) generations.
Keywords:
adverse outcome pathwayhistopathologyperfluorooctanesulfonic acid (PFOS)transcriptomicszebrafish

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  • Histopathological analysis was conducted to assess liver tissue changes, including vacuolation.
  • RNA sequencing (RNAseq) was employed to analyze gene expression patterns and identify affected metabolic pathways.

    • Main Results:

    • High PFOS exposure (100 µg/L) significantly increased hepatocellular vacuolation in both P and F1 generations, with more severe effects in F1.
    • RNAseq revealed a greater number of affected transcripts in the F1 generation (955) compared to the P generation (103), particularly at high PFOS concentrations.
    • PFOS exposure disrupted lipid metabolism pathways, including cholesterol biosynthesis and the PPAR pathway, correlating with observed lipid accumulation and steatosis.

    Conclusions:

    • PFOS exposure induces significant hepatotoxicity and disrupts lipid metabolism in zebrafish in a dose-dependent and transgenerational manner.
    • The study identified key molecular pathways involved in PFOS-induced liver damage, supporting the development of an AOP for liver steatosis.
    • These findings underscore the environmental and health risks associated with PFOS contamination and highlight the importance of studying multi-generational effects.