ArticleiScience2026
PFOS and PFOA exposure induces liver injury and sex-dependent immune effects in C57BL/6 mice.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Perfluorooctanoic acid exposure disrupts gut microbiota and aggravates experimental colitis.Environmental pollution (Barking, Essex : 1987) · 2026Article
- A human PBMC-based new approach method reveals PFAS-driven T-cell proliferation and immune dysregulation.Archives of toxicology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Per- and polyfluoroalkyl substances (PFASs) are persistent environmental contaminants. Perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS), representing carboxylate and sulfonate subclasses, are among the most frequently detected PFASs in biomonitoring studies. We characterized the hepatotoxicity and immunotoxicity of PFOS and PFOA in male and female C57BL/6-Elite mice exposed via oral gavage for 28 (1.5 mg/kg/day) or 56 days (0.166-1.5 mg/kg/day). Both compounds caused pancreatic atrophy, hepatomegaly, elevated serum biomarkers of liver injury, and decreased serum triglyceride levels across sexes and exposure durations. Liver transcriptomics revealed enrichment of PPAR signaling, lipid metabolism disruption, and AGE-RAGE pathways. Immunotoxicity assessments showed PFOS-induced cytokine suppression (interleukin-4 [IL-4], IL-17α, tumor necrosis factor-alpha [TNF-α], and monocyte chemoattractant protein-1 [MCP-1]) in males, while females exhibited minimal cytokine changes but altered thymocyte development. Overall, PFASs caused sex-independent hepatic and pancreatic toxicity but sex-dependent immune effects. Limitations include asymmetric dosing and lack of estrous monitoring; future studies should integrate histopathology and gene expression confirmatory analysis.
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Registered trials
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