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ダイオキシン類の発がん性への影響
https://az.repo.nii.ac.jp/records/4693
https://az.repo.nii.ac.jp/records/4693425380bc-d5b0-44ab-bfb1-d8cc78f2c906
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
bull_jau_vol9-10-246.pdf (126.4 kB)
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| Item type | 紀要論文 / Departmental Bulletin Paper(1) | |||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|
| 公開日 | 2004-01-01 | |||||||||||
| タイトル | ||||||||||||
| タイトル | ダイオキシン類の発がん性への影響 | |||||||||||
| タイトル | ||||||||||||
| タイトル | Effects of Exposure to Dioxins, as Endocrine Disruptors, on Carcinogenesis. : Mechanism and its regulation of dioxins-induced carcinogenesis(Research Group 6) | |||||||||||
| 言語 | en | |||||||||||
| 言語 | ||||||||||||
| 言語 | jpn | |||||||||||
| 資源タイプ | ||||||||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||||||||
| 資源タイプ | departmental bulletin paper | |||||||||||
| ページ属性 | ||||||||||||
| 内容記述タイプ | Other | |||||||||||
| 内容記述 | P(論文) | |||||||||||
| 記事種別 | ||||||||||||
| 内容記述タイプ | Other | |||||||||||
| 内容記述 | 特集 | |||||||||||
| Type | ||||||||||||
| 内容記述タイプ | Other | |||||||||||
| 内容記述 | FEATURE ARTICLES | |||||||||||
| 著者 |
和久井, 信
× 和久井, 信
× Wakui, Shin
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| 著者ID | ||||||||||||
| 000073 | ||||||||||||
| Author ID | ||||||||||||
| 000073 | ||||||||||||
| 所属機関 | ||||||||||||
| 獣医学部 | ||||||||||||
| Institution or Company | ||||||||||||
| School of Veterinary Medicine | ||||||||||||
| 抄録 | ||||||||||||
| 内容記述タイプ | Abstract | |||||||||||
| 内容記述 | 比較的低用量PCB126胎生期曝露群のラットでは,DMBA投与後の肝臓におけるCYP1B1発現亢進することが明らかとなった。この結果は,比較的低用量PCB126胎生期曝露群のラットでは,生後50日齢において有意に発がん性の高い体内環境になっていることが示唆された。 | |||||||||||
| Abstract | ||||||||||||
| 内容記述タイプ | Other | |||||||||||
| 内容記述 | Previously we reported finding that prenatal exposure to a relatively low dose of 3,3',4,4',5-pentacholobiphenyl (PCB126) increases the rats with DMBA-induced mammary carcinoma, while a high dose decreases it. One of the most important factors determining sensitivity of the mammary carcinogenesis is its metabolic stage of carcinogenic agent. DMBA is an indirect carcinogen that requires host metabolism to yield its ultimate carcinogenic form, and this metabolism is conducted by cytochrome P450 1A1 and 1B1 (CYP1). Hence, we investigated the hepatic CYP1 expression following DMBA (100mg/kg b.w.) injection (i.g.) to 50-day-old offsprings of female SD rats were injected (i.g.) with 2.5ng, 250ng, 7.5μg of PCB126/kg, or the vehicle, on days 13 to 19 postconception. At 6 hr after DMBA injection, CYP1 mRNA significantly increased all PCB treated groups. The 7.5ug-group revealed high level CYP1A1 mRNA until Day 20 after DMBA injection, and that of CYP1B1 mRNA until Day 2. While the 250 ng-group revealed high level CYP1A1 mRNA until Day 2, and that of CYP1B1 mRNA until Day 20. The 2.5 ng- revealed higher level of CYP1 mRNA until Day 2 compared to the vehicle-group. Expression of protein level of CYP1 was similar to that of each mRNA level. Thus prenatal exposure to a relatively low dose of PCB126 induced a prolongation of expression in CYP1B1 mRNAs. Since the DMBA oxidation produces the highly mutagenic metabolite and is finally catalyzed by CYP1B1, a relatively low PCB126 dose-group might be acquired the biological character potentially increase the risk of DMBA-induced mammary carcinoma. | |||||||||||
| 書誌情報 |
麻布大学雑誌 en : Journal of Azabu University 巻 9/10, p. 246-247, 発行日 2005-03-31 |
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| レポート・演題番号 | ||||||||||||
| 内容記述タイプ | Other | |||||||||||
| 内容記述 | 麻布大学ハイテク・リサーチ・センター研究プロジェクト 研究サブ・グループ6 | |||||||||||
| 出版者 | ||||||||||||
| 出版者 | 麻布大学 | |||||||||||
| Publisher | ||||||||||||
| 出版者 | Azabu University | |||||||||||
| ISSN | ||||||||||||
| 収録物識別子タイプ | ISSN | |||||||||||
| 収録物識別子 | 1346-5880 | |||||||||||
| 書誌レコードID | ||||||||||||
| 収録物識別子タイプ | NCID | |||||||||||
| 収録物識別子 | AA11561468 | |||||||||||
| 著者版フラグ | ||||||||||||
| 出版タイプ | VoR | |||||||||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||||||||
| text version | ||||||||||||
| 出版タイプ | VoR | |||||||||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||||||||
| format | ||||||||||||
| 内容記述タイプ | Other | |||||||||||
| 内容記述 | application/pdf | |||||||||||
