The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
Immunotoxicity of Perfluorooctanoic Acid and Perfluorooctane Sulfonate and the Role of Peroxisome Proliferator-Activated Receptor Alpha
Abstract
Perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) are environmentally widespread and persistent chemicals with multiple toxicities reported in experimental animals and humans. These compounds can trigger biological activity by activating the alpha isotype of peroxisome proliferator-activated receptors (PPARs), ligand-activated transcription factors that regulate gene expression; however, some biological effects may occur independently of the receptor. Activation of the peroxisome proliferator-activated receptor alpha (PPARalpha) modulates lipid and glucose homeostasis, cell proliferation and differentiation, and inflammation. Reported immunomodulation in experimental animals exposed to PFOA and PFOS has included altered inflammatory responses, production of cytokines and other proteins, reduced lymphoid organ weights, and altered antibody synthesis. Mounting experimental animal evidence suggests PPARalpha independence of some immune effects. This evidence originates primarily from studies with PPARalpha knockout models exposed to PFOA that demonstrate hepatic peroxisome proliferation, reduced lymphoid organ weights, and altered antibody synthesis. As human PPARalpha expression is significantly less than that of rodents, potential PPARalpha independence indicates that future research must explore mechanisms of action of these compounds, including PPARalpha-dependent and -independent pathways. This multiauthored review contains brief descriptions of current and recently published work exploring immunomodulation by PFOA and PFOS, as well as a short overview of other PPARalpha ligands of therapeutic and environmental interest.
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Citations
Cites
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“In the context of the current model of M1/M2 macrophage subsets (Mosser, 2003), the data with DEHP and clofibrate support the conclusion that PPARα ligands may induce a reprogramming of macrophage inflammatory potential toward the antiinflammatory M2-phenotype.”
BackgroundThe PPARs: From Orphan Receptors to Drug Discovery
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The toxicology of perfluorooctanoate
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Cited by
Epidemiologic Evidence on the Health Effects of Perfluorooctanoic Acid (PFOA)
Steenland, K., Fletcher, T., & Savitz, D. A. (2010) · Environmental Health Perspectives · doi:10.1289/ehp.0901827 · Cited by 660
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“…volume 122 | number 10 | October 2014 1029 there have been inconsistent conclusions about the evidence of an association between PFOA and fetal growth (DeWitt et al. 2009; Hekster et al. 2003; Jensen and Leffers 2008; Kennedy et al. 2004; Kudo and Kawashima 2003; Lau et al. 2004, 2007; Lindstrom…”
BackgroundImmunotoxicity of Perfluorinated Compounds: Recent Developments
DeWitt, J. C., Peden-Adams, M. M., Keller, J. M., & Germolec, D. R. (2012) · Toxicologic Pathology · doi:10.1177/0192623311428473 · Cited by 457
Self-citation
Metadata
- Authors
- DeWitt, J. C., Shnyra, A., Badr, M. Z., Loveless, S. E., Hoban, D., Frame, S. R., Cunard, R., Anderson, S. E., Meade, B. J., Peden-Adams, M. M., Luebke, R. W., & Luster, M. I.
- Venue
- Critical Reviews in Toxicology
- Publisher
- Informa UK Limited
- Published
- 2009-01
- Volume
- 39
- Issue
- 1
- Pages
- 76-94
- ISSN
- 0045-6446 (ISSN-L)
- 1040-8444
- 1547-6898
- OpenAlex
- W2099251250
- Cited by
- 266
- References
- 11
- FWCI
- 9.35
- Type
- journal article
- Language
- en
- Open access
- closed
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- DeWitt, J. C., Shnyra, A., Badr, M. Z., Loveless, S. E., Hoban, D., Frame, S. R., Cunard, R., Anderson, S. E., Meade, B. J., Peden-Adams, M. M., Luebke, R. W., & Luster, M. I. (2009). Immunotoxicity of Perfluorooctanoic Acid and Perfluorooctane Sulfonate and the Role of Peroxisome Proliferator-Activated Receptor Alpha. Critical Reviews in Toxicology. https://doi.org/10.1080/10408440802209804
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
