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乙醇和乙醛对大鼠经二乙基亚硝胺启动的癌前谷胱甘肽S-转移酶P型阳性肝细胞灶发展的修饰作用

Modification potentials of ethyl alcohol and acetaldehyde on development of preneoplastic glutathione S-transferase P-form-positive liver cell foci initiated by diethylnitrosamine in the rat.

作者信息

Ikawa E, Tsuda H, Sakata T, Masui T, Satoh K, Sato K, Ito N

出版信息

Cancer Lett. 1986 Apr;31(1):53-60. doi: 10.1016/0304-3835(86)90166-7.

DOI:10.1016/0304-3835(86)90166-7
PMID:3697954
Abstract

The modification potentials of ethyl alcohol (EA) and acetaldehyde (AA) on development of immunohistochemical glutathione S-transferase (placental type)-positive (GST-P+) liver cell foci were examined in an in vivo short-term assay system. Rats were given a single intraperitoneal injection of diethylnitrosamine (DEN) and then various concentrations of EA (20, 10, 5%) or AA (5, 2.5%) in their drinking water from week 2 till termination in week 6. All rats were subjected to two-thirds partial hepatectomy in week 3. Animals given EA (20% and 10%) or AA showed significant decrease in liver and body weight. However, only EA caused significant dose-related inhibition of development of areas of foci (mm2/cm2), but AA had no effect on their development.

摘要

在一个体内短期检测系统中,研究了乙醇(EA)和乙醛(AA)对免疫组化谷胱甘肽S-转移酶(胎盘型)阳性(GST-P+)肝细胞灶发展的修饰潜力。给大鼠腹腔注射一次二乙基亚硝胺(DEN),然后从第2周直到第6周处死,在它们的饮用水中加入不同浓度的EA(20%、10%、5%)或AA(5%、2.5%)。所有大鼠在第3周接受了三分之二部分肝切除术。给予EA(20%和10%)或AA的动物肝脏和体重显著下降。然而,只有EA引起了灶面积(mm2/cm2)发展的显著剂量相关抑制,而AA对其发展没有影响。

相似文献

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Modification potentials of ethyl alcohol and acetaldehyde on development of preneoplastic glutathione S-transferase P-form-positive liver cell foci initiated by diethylnitrosamine in the rat.乙醇和乙醛对大鼠经二乙基亚硝胺启动的癌前谷胱甘肽S-转移酶P型阳性肝细胞灶发展的修饰作用
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2
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引用本文的文献

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Long-term ethanol consumption promotes hepatic tumorigenesis but impairs normal hepatocyte proliferation in rats.长期乙醇摄入可促进大鼠肝肿瘤发生,但损害正常肝细胞增殖。
J Nutr. 2011 Jun;141(6):1049-55. doi: 10.3945/jn.110.136531. Epub 2011 Apr 13.
2
Enhancing effect of ethanol on aflatoxin B1-induced hepatocarcinogenesis in male ACI/N rats.乙醇对雄性 ACI/N 大鼠黄曲霉毒素 B1 诱导的肝癌发生的增强作用。
Jpn J Cancer Res. 1989 Jun;80(6):526-30. doi: 10.1111/j.1349-7006.1989.tb01671.x.