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PPAR Research
Volume 2008, Article ID 759716, 12 pages
Review Article

PPAR - and DEHP-Induced Cancers

Department of Occupational and Environmental Health, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan

Received 12 April 2008; Accepted 8 July 2008

Academic Editor: Dipak Panigrahy

Copyright © 2008 Yuki Ito and Tamie Nakajima. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Di(2-ethylhexyl)phthalate (DEHP) is a widely used plasticizer and a potentially nongenotoxic carcinogen. Its mechanism had been earlier proposed based on peroxisome proliferator-activated receptor (PPAR ) because metabolites of DEHP are agonists. However, recent evidence also suggests the involvement of non-PPAR multiple pathway in DEHP-induced carcinogenesis. Since there are differences in the function and constitutive expression of PPAR among rodents and humans, species differences are also thought to exist in the carcinogenesis. However, species differences were also seen in the lipase activity involved in the first step of the DEHP metabolism, which should be considered in DEHP-induced carcinogenesis. Taken together, it is very difficult to extrapolate the results from rodents to humans in the case of DEHP carcinogenicity. However, PPAR -null mice or mice with human PPAR gene have been developed, which may lend support to make such a difficult extrapolation. Overall, further mechanical study on DEHP-induced carcinogenicity is warranted using these mice.