A Reexamination of the PPAR-α Activation Mode of Action as a Basis for Assessing Human Cancer Risks of Environmental Contaminants | Zendy

Kathryn Z. Guyton | Zendy; Weihsueh A. Chiu | Zendy; Thomas F. Bateson | Zendy; Jennifer Jinot | Zendy; Cheryl Siegel Scott | Zendy; Rebecca C. Brown | Zendy; Jane C. Caldwell | Zendy

Open Access

A Reexamination of the PPAR-α Activation Mode of Action as a Basis for Assessing Human Cancer Risks of Environmental Contaminants

Author(s) -

Kathryn Z. Guyton,

Weihsueh A. Chiu,

Thomas F. Bateson,

Jennifer Jinot,

Cheryl Siegel Scott,

Rebecca C. Brown,

Jane C. Caldwell

Publication year - 2009

Publication title -

environmental health perspectives

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.257

H-Index - 282

eISSN - 1552-9924

pISSN - 0091-6765

DOI - 10.1289/ehp.0900758

Subject(s) - peroxisome proliferator activated receptor , carcinogen , peroxisome proliferator activated receptor alpha , mode of action , nuclear receptor , alpha (finance) , peroxisome , biology , receptor , toxicology , medicine , biochemistry , transcription factor , gene , construct validity , nursing , patient satisfaction

Diverse environmental contaminants, including the plasticizer di(2-ethylhexyl)phthalate (DEHP), are hepatocarcinogenic peroxisome proliferators in rodents. Peroxisome proliferator-activated receptor-alpha (PPAR-alpha) activation and its sequelae have been proposed to constitute a mode of action (MOA) for hepatocarcinogenesis by such agents as a sole causative factor. Further, based on a hypothesized lower sensitivity of humans to this MOA, prior reviews have concluded that rodent hepatocarcinogenesis by PPAR-alpha agonists is irrelevant to human carcinogenic risk.

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