Reporter gene mutation in the livers of gpt delta mice treated with 5-(hydroxymethyl)-2-furfural, a contaminant of various foods
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- Matsushita Kohei
- Division of Pathology, National Institute of Health Sciences
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- Ishii Yuji
- Division of Pathology, National Institute of Health Sciences
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- Kijima Aki
- Division of Pathology, National Institute of Health Sciences
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- Jin Meilan
- Division of Pathology, National Institute of Health Sciences
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- Takasu Shinji
- Division of Pathology, National Institute of Health Sciences
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- Kuroda Ken
- Division of Pathology, National Institute of Health Sciences
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- Kodama Yukio
- Division of Toxicology, National Institute of Health Sciences
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- Ogawa Kumiko
- Division of Pathology, National Institute of Health Sciences
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- Umemura Takashi
- Division of Pathology, National Institute of Health Sciences
書誌事項
- タイトル別名
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- Reporter gene mutation in the livers of <i>gpt</i> delta mice treated with 5-(hydroxymethyl)-2-furfural, a contaminant of various foods
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抄録
A major product formed during the Maillard reaction is 5-(hydroxymethyl)-2-furfural (HMF), which is present in various foods and beverages such as honey and fruit juice. HMF was shown to be a hepatocarcinogen in female mice using long-term bioassays. Although HMF is not a mutagen in conventional in vitro mutation assays, 5-sulfoxymethylfurfural (SMF), a reactive metabolite of HMF produced following sulfotransferase conjugation, does show mutagenicity. Thus, HMF-induced hepatocarcinogenesis likely involves genotoxic mechanisms. To clarify the mechanisms underlying HMF-induced hepatocarcinogenesis, female B6C3F1 gpt delta mice were given HMF at carcinogenic doses (188 or 375 mg/kg b.w.) by gavage for 5 days per week for 4 weeks. This treatment produced no significant differences in mutant frequencies (MFs) of gpt and red/gam (Spi-) genes among the groups. These results suggest that genotoxicity does not contribute to HMF-induced hepatocarcinogenesis. Parameters related to cell proliferation, such as proliferation cell nuclear antigen-labeling index and Cyclin D1 and E1 mRNA expression, exhibited no significant changes in the livers of HMF-treated groups. In view of the lack of carcinogenicity in rats, HMF may be considered to be a weak carcinogen. These results help us to understand the underlying mechanisms of action of HMF carcinogenesis.
収録刊行物
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- The Journal of Toxicological Sciences
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The Journal of Toxicological Sciences 37 (5), 1077-1082, 2012
一般社団法人 日本毒性学会
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詳細情報 詳細情報について
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- CRID
- 1390001204905705984
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- NII論文ID
- 130004446998
- 10030876846
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- NII書誌ID
- AN00002808
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- COI
- 1:STN:280:DC%2BC3s%2Fis1OmtA%3D%3D
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- ISSN
- 18803989
- 03881350
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- NDL書誌ID
- 024030456
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- PubMed
- 23038016
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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
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可