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Dibutylphthalate (DBP), di(2-ethylhexyl)phthalate (DEHP), and di(2-ethylhexyl)adipate (DEHA) are used as plasticizers. Their metabolites activate peroxisome proliferator-activated receptor (PPAR)  α , which may be related to their toxicities. However, species differences in the receptor functions between rodents and human make it difficult to precisely extrapolate their toxicity from animal studies to human. In this paper, we compared the species differences in the activation of mouse and human hepatic PPAR α  by these plasticizers using wild-type ( mPPARα ) and humanized  PPARα  ( hPPARα ) mice. At 12 weeks old, each genotyped male mouse was classified into three groups, and fed daily for 2 weeks per os with corn oil (vehicle control), 2.5 or 5.0 mmol/kg DBP (696, 1392 mg/kg), DEHP (977, 1953 mg/kg), and DEHA (926, 1853 mg/kg), respectively. Generally, hepatic PPAR α  of  mPPARα  mice was more strongly activated than that of  hPPARα  mice when several target genes involving  β -oxidation of fatty acids were evaluated. Interestingly, all plasticizers also activated hepatic constitutive androstane receptor (CAR) more in  hPPARα  mice than in  mPPARα  mice. Taken together, these plasticizers activated mouse and human hepatic PPAR α  as well as CAR. The activation of PPAR α  was stronger in  mPPARα  mice than in  hPPARα  mice, while the opposite was true of CAR.

ppar research

Plasticizers May Activate Human Hepatic Peroxisome Proliferator-Activated Receptor<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mi mathvariant="bold">α</mml:mi></mml:math>Less Than That of a Mouse but May Activate Constitutive Androstane Receptor in Liver

Plasticizers May Activate Human Hepatic Peroxisome Proliferator-Activated ReceptorαLess Than That of a Mouse but May Activate Constitutive Androstane Receptor in Liver