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停止长期喂食二乙基亚硝胺对成年大鼠肝癌发生的影响。

Effects of discontinuation of chronic feeding of diethylnitrosamine on the development of hepatomas in adult rats.

作者信息

Barbason H, Smoliar V, Fridman-Manduzio A, Betz E H

出版信息

Br J Cancer. 1979 Aug;40(2):260-7. doi: 10.1038/bjc.1979.174.

DOI:10.1038/bjc.1979.174
PMID:475971
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2010017/
Abstract

Diethylnitrosamine (DENA) at 10 mg/kg was fed to adult rats either continuously or for periods ranging from 1 to 10 weeks. Survival correlated inversely with the duration of carcinogen feeding. Less than 4 weeks of DENA feeding produced only preneoplastic foci that persisted indefinitely; 4 weeks were found to be necessary for the transformation of preneoplastic lesions into liver cancers; after 6 weeks, the incidence of hepatomas was 100%. The process of liver cancerization appeared to be identical whether DENA was fed for 8 weeks or continuously up to the time of death. These results are discussed in the light of the evolution of the homoeostatic control of liver-cell division during DENA feeding, in order to distinguish the different successive roles played by the carcinogen.

摘要

将10毫克/千克的二乙基亚硝胺(DENA)持续或在1至10周的时间段内喂给成年大鼠。存活率与致癌物喂养的持续时间呈负相关。少于4周的DENA喂养仅产生可无限期持续的癌前病灶;发现4周是癌前病变转化为肝癌所必需的;6周后,肝癌的发生率为100%。无论DENA是喂养8周还是持续到死亡时,肝癌形成过程似乎都是相同的。根据DENA喂养期间肝细胞分裂稳态控制的演变来讨论这些结果,以便区分致癌物所起的不同连续作用。

相似文献

1
Effects of discontinuation of chronic feeding of diethylnitrosamine on the development of hepatomas in adult rats.停止长期喂食二乙基亚硝胺对成年大鼠肝癌发生的影响。
Br J Cancer. 1979 Aug;40(2):260-7. doi: 10.1038/bjc.1979.174.
2
Proliferation of preneoplastic lesions after discontinuation of chronic DEN feeding in the development of hepatomas in rat.在大鼠肝癌发生过程中,停止长期给予二乙基亚硝胺(DEN)后,癌前病变的增殖情况。
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Liver cell control after discontinuation of DENA feeding in hepatocarcinogenesis.肝癌发生过程中停止给予二乙基亚硝胺后肝细胞的控制
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A subnecrogenic dose of diethylnitrosamine is able to initiate hepatocarcinogenesis in the rat when coupled with fasting/refeeding.当与禁食/再喂养相结合时,亚致癌剂量的二乙基亚硝胺能够引发大鼠的肝癌发生。
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Hepatic foci of cellular and enzymatic alteration and nodules in rats treated with clofibrate or diethylnitrosamine followed by phenobarbital: their rate of onset and their reversibility.用氯贝丁酯或二乙基亚硝胺处理后再用苯巴比妥处理的大鼠肝脏细胞和酶改变灶及结节:它们的发生速率和可逆性。
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Enzyme pattern and growth rate of liver preneoplastic clones during carcinogenesis by diethylnitrosamine.二乙基亚硝胺致癌过程中肝脏癌前克隆的酶谱和生长速率
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引用本文的文献

1
Promotion mechanism of phenobarbital and partial hepatectomy in DENA hepatocarcinogenesis cell kinetics effect.苯巴比妥和部分肝切除术在二乙基亚硝胺诱导肝癌发生中细胞动力学效应的促进机制
Br J Cancer. 1983 Apr;47(4):517-25. doi: 10.1038/bjc.1983.82.

本文引用的文献

1
Liver carcinogenesis by diethylnitrosamine in the rat.大鼠中由二乙基亚硝胺引起的肝癌发生
Science. 1966 Apr 1;152(3718):83-5. doi: 10.1126/science.152.3718.83.
2
Persistent changes induced by subcarcinogenic doses of 3'-methyl-4-(dimethylamino)azobenzene in rat liver.亚致癌剂量的3'-甲基-4-(二甲基氨基)偶氮苯在大鼠肝脏中诱导的持续性变化。
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3
Liver cell responses to the carcinogen 3'-methyl-4-dimethylaminoazobenzene.肝细胞对致癌物3'-甲基-4-二甲基氨基偶氮苯的反应。
Chem Biol Interact. 1970 Feb;1(3):301-5. doi: 10.1016/0009-2797(70)90016-5.
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Specific stages of cellular response to homeostatic control during diethylnitrosamine-induced liver carcinogenesis.二乙基亚硝胺诱导肝癌发生过程中细胞对稳态控制反应的特定阶段
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Growth kinetics of diethylnitrosamine-induced, enzyme-deficient "preneoplastic" liver cell populations in vivo and in vitro.二乙基亚硝胺诱导的、酶缺陷型“癌前”肝细胞群体在体内和体外的生长动力学
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Probable clonal genesis of cellular islands induced in rat liver by diethylnitrosamine.二乙基亚硝胺诱导大鼠肝脏中细胞岛的可能克隆起源。
Eur J Cancer (1965). 1971 Aug;7(4):369-71. doi: 10.1016/0014-2964(71)90083-1.
8
Quantitative study on foci of altered liver cells induced in the rat by a single dose of diethylnitrosamine and partial hepatectomy.单剂量二乙基亚硝胺及部分肝切除诱导大鼠肝细胞改变灶的定量研究
J Natl Cancer Inst. 1972 Jul;49(1):93-106.
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Influence of a chronic administration of diethylnitrosamine on the relation between specific tissular and division functions in the rat liver.
Eur J Cancer (1965). 1975 Aug;11(8):531-6. doi: 10.1016/0014-2964(75)90124-3.
10
Comparative enhancing effects of phenobarbital, amobarbital, diphenylhydantoin, and dichlorodiphenyltrichloroethane on 2-acetylaminofluorene-induced hepatic tumorigenesis in the rat.苯巴比妥、异戊巴比妥、苯妥英和滴滴涕对大鼠2-乙酰氨基芴诱导的肝脏肿瘤发生的比较增强作用。
Cancer Res. 1975 Oct;35(10):2884-90.