Molecular analysis on the possible mechanism of β-naphthoflavone-induced hepatocarcinogenesis in rats
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- Yokouchi Yusuke
- Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology
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- Muguruma Masako
- Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology
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- Moto Mitsuyoshi
- Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology
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- Takahashi Miwa
- Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology
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- Jin Meilan
- Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology
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- Kenmochi Yusuke
- Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology
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- Kohno Taichi
- Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology
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- Dewa Yasuaki
- Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology
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- Mitsumori Kunitoshi
- Laboratory of Veterinary Pathology, Tokyo University of Agriculture and Technology
書誌事項
- タイトル別名
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- Molecular Analysis on the Possible Mechanism of .BETA.-Naphthoflavone-Induced Hepatocarcinogenesis in Rats
- Molecular analysis on the possible mechanism of b naphthoflavone induced hepatocarcinogenesis in rats
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説明
It has been speculated that oxidative stress is involved in the liver tumor-promoting effect of β-naphthoflavone (BNF; 5,6-benzoflavone) in rats, because of its strong induction of cytochrome P450 (CYP) 1A enzymes. In order to clarify the mechanism of liver tumor promoting effects of BNF, male F344 rats were initiated with a single intraperitoneal injection of 200 mg/kg diethylnitrosamine (DEN), and fed diet containing 2% of BNF for 6 weeks staring 2 weeks after injection. Two/third partial hepatectomy was perfomed at Week 3 after the treatment of BNF. Low-density Rat Toxicology & Drug Resistance Microarray and quantitative analyses of mRNA expressions of the selected genes using real-time reverse transcription (RT) -PCR were carried out on total RNAs extracted from the livers of F344 rats. Collected liver tissues were subjected to light microscopic examinations (hematoxylin and eosin staining), immunohistochemistries of proliferating cell nuclear antigen (PCNA), glutathione S-transferase placental form (GST-P) and CYP1A1, and Schmorl staining to identify lipofuscin. Gene expression analysis showed that 7 genes (CYP1A1, CYP1A2, CYP1B1, Gstm2 (GST mu2), Gstm3, glutathione peroxidase (Gpx)2 and NAD(P)H dehydrogenase, quinone 1(Nqo1)) were up-regulated (> 1.5 fold), and 4 genes (8-oxoguanine DNA glycosylase (Ogg1), Gpx1, peroxiredoxin (Prdx) 1 and P450 oxidoreductase (Por)) were down-regulated (< 0.67 fold) in the DEN + BNF group rats as compared with the DEN alone group. In immunohistochemical analyses, the numbers of foci positive for GST-P, the rate of PCNA-positive cells, and the rate of CYP1A1-positive cells were significantly increased in the DEN + BNF group, as compared to the corresponding control. Furthermore, deposition of lipofuscin, positive for Schmorl staining, was moderately increased in the DEN + BNF group. These results confirm the possibility that oxidative stress is involved in the liver tumor-promoting effect of BNF in rats.
収録刊行物
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- Journal of Toxicologic Pathology
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Journal of Toxicologic Pathology 20 (1), 29-37, 2007
日本毒性病理学会
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詳細情報 詳細情報について
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- CRID
- 1390282679391699712
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- NII論文ID
- 10025853784
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- NII書誌ID
- AA12022786
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- ISSN
- 1881915X
- 09149198
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- NDL書誌ID
- 8766742
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDLサーチ
- Crossref
- CiNii Articles
- OpenAIRE
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- 使用不可