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Carcinogenesis, Vol. 21, No. 4, 677-682, April 2000
© 2000 Oxford University Press

Carcinogenesis

Sex-dependent regulation of hepatic peroxisome proliferation in mice by trichloroethylene via peroxisome proliferator-activated receptor {alpha} (PPAR{alpha})

Tamie Nakajima6, Yuji Kamijo1, Nobuteru Usuda2, Yan Liang2, Yoshimitsu Fukushima, Kiyokazu Kametani4, Frank J. Gonzalez5 and Toshifumi Aoyama3

1 Department of Hygiene, Second Department of Internal Medicine,
2 First Department of Anatomy,
3 Department of Aging Biochemistry and
4 General Research Laboratory, Shinshu University School of Medicine, Matsumoto, Nagano 390-8621, Japan and
5 Laboratory of Metabolism, National Cancer Institute, Bethesda, MD 20892, USA

The mechanism of trichloroethylene-induced liver peroxisome proliferation and the sex difference in response was investigated using wild-type Sv/129 and peroxisome proliferator-activated receptor {alpha} (PPAR{alpha})-null mice. Trichloroethylene treatment (0.75 g/kg for 2 weeks by gavage) resulted in liver peroxisome proliferation in wild-type mice, but not in PPAR{alpha}-null mice, suggesting that trichloroethylene-induced peroxisome proliferation is primarily mediated by PPAR{alpha}. No remarkable sex difference was observed in induction of peroxisome proliferation, as measured morphologically, but a markedly higher induction of several enzymes and PPAR{alpha} protein and mRNA was found in males. On the other hand, trichloroethylene induced liver cytochrome P450 2E1, the principal enzyme responsible for metabolizing trichloroethylene to chloral hydrate, only in males, which resulted in similar expression levels in both sexes after the treatment. Trichloroethylene influenced neither the level of catalase, an enzyme involved in the reduction of oxidative stress, nor aldehyde dehydrogenase, the main enzyme catalyzing the conversion to trichloroacetic acid. These results suggest that trichloroethylene treatment causes a male-specific PPAR{alpha}-dependent increase in cellular oxidative stress.


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