Enhancing effect of phenobarbital on the development of enzyme-altered islands and hepatocellular carcinomas initiated by 3'-methyl-4-(dimethylamino) azobenzene or diethylnitrosamine.
Enhancing effect of phenobarbital on the development of enzyme-altered islands and hepatocellular carcinomas initiated by 3'-methyl-4-(dimethylamino) azobenzene or diethylnitrosamine.
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苯巴比妥对 3-甲基-4-（二甲氨基）偶氮苯或二乙基亚硝胺引发的酶改变岛和肝细胞癌的发展具有增强作用。
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发表时间：
1978
期刊：
影响因子：
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通讯作者：
H. Sugano
中科院分区：
文献类型：
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作者：
T. Kitagawa;H. Sugano
本文研究了膳食苯巴比妥对3 ′-甲基-4-（二甲氨基）偶氮苯（3 ′-Me-DAB）或二乙基亚硝胺（DENA）短期处理引起的大鼠酶改变岛（EAI）和肝细胞癌的影响。苯巴比妥普遍增强致癌物诱导（酶改变）细胞的增殖，使EAI的数量和大小在早期阶段比对照组保持在基础饮食中的苯巴比妥喂养组大得多。然而，EAI的生长速度并不均匀，只有少数进展为大岛或癌。在最初用3 ′-Me-DAB处理3周的组中，苯巴比妥对癌产生的增强作用在第36周时是显著的，而在用3 ′-Me-DAB处理1周的组中，尽管出现了大量的小EAI，但在第60周时没有癌发生。因此，即使在短时间内给予致癌物作为引发剂时，也观察到致癌物的总和效应。苯巴比妥的增强作用在DENA启动的组中也很明显，然而，在对照组中也有相当数量的癌发生。致癌物诱导的细胞或EAI作为群体，根据引发剂的不同，在发展成癌的潜力方面表现出固有的不同。
Effect of dietary phenobarbital on the development of enzyme-altered islands (EAI) and hepatocellular carcinomas initiated by a short-term treatment with 3'-methyl-4-(dimethylamino) azobenzene (3'-Me-DAB) or diethylnitrosamine (DENA) in the rat was studied. Phenobarbital generally enhanced the proliferation of carcinogen-induced (enzyme-altered) cells so that the number and size of EAI were much larger in phenobarbital-fed groups in early stages than in control groups kept on a basal diet. The growth rate of EAI was, however, not uniform and only a small minority progressed to large islands or carcinomas. In groups initially treated with 3'-Me-DAB for 3 weeks, the enhancing effect of phenobarbital on cancer production was remarkable by the 36th week whereas in groups treated with 3'-Me-DAB for 1 week, no cancer developed by the 60th week, although a large number of small EAI appeared. Thus a summation effect of the carcinogen was observed even when the carcinogen was given for a short period as an initiator. The enhancing effect of phenobarbital was also marked in the groups initiated by DENA, in which, however, considerable number of carcinomas developed in control groups also. The carcinogen-induced cells or EAI appeared inherently different, as the population, in the potentiality to progress to carcinoma according to the difference of an initiator.