Trichloroethylene liver toxicity in mouse and rat: microarray analysis reveals species differences in gene expression

被引：32

作者：

Sano, Yuri ^{[1
]}

Nakashima, Hiroshi ^{[2
]}

Yoshioka, Noriyuki ^{[1
]}

Etho, Norihito ^{[3
]}

Nomiyama, Tetsuo ^{[4
]}

Nishiwaki, Yuji ^{[1
]}

Takebayashi, Toru ^{[1
]}

Oame, Kazuyuki ^{[1
]}

机构：

[1] Keio Univ, Sch Med, Dept Prevent Med & Publ Hlth, Tokyo, Japan

[2] Natl Def Med Coll, Dept Prevent Med & Publ Hlth, Tokorozawa, Saitama 359, Japan

[3] Tokai Univ, Dept Biomed Engn, Sch High Technol Human Welf, Numazu, Japan

[4] Shinshu Univ, Sch Med, Dept Prevent Med & Publ Hlth, Matsumoto, Nagano 390, Japan

来源：

ARCHIVES OF TOXICOLOGY | 2009年 / 83卷 / 09期

关键词：

PEROXISOME PROLIFERATORS; KUPFFER CELLS; SIGNALING PATHWAY; TUMOR INDUCTION; JNK ACTIVATION; PPAR-ALPHA; IN-VIVO; KAPPA-B; TRICHLOROACETATE; DICHLOROACETATE;

D O I：

10.1007/s00204-009-0431-1

中图分类号：

R99 [毒物学（毒理学）];

学科分类号：

100405 [卫生毒理学];

摘要：

Trichloroethylene (TCE), an industrial organic solvent found in the environment, is a known carcinogen in laboratory animals and is believed to be carcinogenic in humans. Its carcinogenicity is subject to species-specific differences in biological activity, causing hepatocellular carcinoma in mouse and renal-cell carcinoma in rat. We have sought to better understand TCE's mode of action (MOA) by studying the alterations in gene expression profiles of liver in mice and rats that were administrated TCE by oral gavage either once or daily for 14 days. Microarray analysis revealed distinct transcriptional profiles and differences in biological pathways not only species-specific, but also pulse-dose effects within each species. For example, inhibition of the TGF-beta pathway and activation of MAPK signaling were specific to mice repeatedly exposed to TCE. A better understanding of the MOA in mice and rats will lead to better hypotheses of TCE's affect on humans.

引用

页码：835 / 849

页数：15

共 39 条

[1]

The transcriptional response to a peroxisome proliferator-activated receptor α agonist includes increased expression of proteome maintenance genes [J].

Anderson, SP ;

Howroyd, P ;

Liu, J ;

Qian, X ;

Bahnemann, R ;

Swanson, C ;

Kwak, MK ;

Kensler, TW ;

Corton, JC .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (50) :52390-52398

[2]

Bojes HK, 1996, CANCER RES, V56, P1

[3]

Proceedings in uncovering the mechanism behind peroxisome proliferator-induced hepatocarcinogenesis [J].

Bosgra, S ;

Mennes, W ;

Seinen, W .

TOXICOLOGY, 2005, 206 (03) :309-323

[4]

LIVER-TUMOR INDUCTION IN B6C3F1 MICE BY DICHLOROACETATE AND TRICHLOROACETATE [J].

BULL, RJ ;

SANCHEZ, IM ;

NELSON, MA ;

LARSON, JL ;

LANSING, AJ .

TOXICOLOGY, 1990, 63 (03) :341-359

[5]

Contribution of dichloroacetate and trichloroacetate to liver tumor induction in mice by trichloroethylene [J].

Bull, RJ ;

Orner, GA ;

Cheng, RS ;

Stillwell, L ;

Stauber, AJ ;

Sasser, LB ;

Lingohr, MK ;

Thrall, BD .

TOXICOLOGY AND APPLIED PHARMACOLOGY, 2002, 182 (01) :55-65

[6]

The E3 ubiquitin ligase itch couples JNK activation to TNFα-induced cell death by inducing c-FLIPL turnover [J].

Chang, LF ;

Kamata, H ;

Solinas, G ;

Luo, JL ;

Maeda, S ;

Venuprasad, K ;

Liu, YC ;

Karin, M .

CELL, 2006, 124 (03) :601-613

[7]

Post-transcriptional control of Cited2 by transforming growth factor β -: Regulation via Smads and Cited2 coding region [J].

Chou, Yu-Ting ;

Yang, Yu-Chung .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2006, 281 (27) :18451-18462

[8]

GenMAPP, a new tool for viewing and analyzing microarray data on biological pathways [J].

Dahlquist, KD ;

Salomonis, N ;

Vranizan, K ;

Lawlor, SC ;

Conklin, BR .

NATURE GENETICS, 2002, 31 (01) :19-20

[9]

BIOCHEMICAL, HISTOLOGICAL, AND ULTRASTRUCTURAL-CHANGES IN RAT AND MOUSE-LIVER FOLLOWING THE ADMINISTRATION OF TRICHLOROETHYLENE - POSSIBLE RELEVANCE TO SPECIES-DIFFERENCES IN HEPATOCARCINOGENICITY [J].

ELCOMBE, CR ;

ROSE, MS ;

PRATT, IS .

TOXICOLOGY AND APPLIED PHARMACOLOGY, 1985, 79 (03) :365-376

[10]

*EUR UN, 2004, 21057 EUR EN EUR CHE, V31

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