Increasing the interval between initiation and the onset of exposure to orotic acid decreases its promoting effect on rat liver carcinogenesis.

Increasing the interval between initiation and the onset of exposure to orotic acid decreases its promoting effect on rat liver carcinogenesis.
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增加乳清酸暴露与开始暴露之间的间隔会降低其对大鼠肝癌发生的促进作用。

DOI:
10.1093/carcin/14.8.1701
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发表时间:
1993
期刊:
影响因子:
4.7
通讯作者:
Sarma,DS
Sarma,DS
中科院分区:
医学2区
文献类型:
--
作者:
Laconi,E;Vasudevan,S;Rao,PM;Rajalakshmi,S;Pani,P;Sarma,DS

文献摘要

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相似文献

本研究旨在确定给予致癌剂后延迟开始促进方案是否会影响乳清酸对大鼠肝细胞癌发展的促进功效。体重130-150 g的雄性Fischer 344大鼠注射单剂量二乙基胺(200 mg/kg体重,腹腔注射),然后分为3组:第1组和第2组在致癌物后1周开始分别给予半合成基础饮食或含1%乳清酸(OA)的相同饮食;第3组在给予二乙基亚硝胺5周后开始接受OA饮食。这 3 组的动物在喂食各自饮食 25、32、42 和 60 周后被处死。结果表明,在致癌物之后延迟开始 OA 饮食可使实验期间不同时间点的肝结节和/或肝细胞癌的发生率降低约 50%。 OA 促进功效的下降显然不能用 OA 缺乏代谢作用来解释,至少在诱导核苷酸库失衡方面是这样,这种情况对于 OA 发挥其肿瘤促进作用似乎很重要。
The present study was designed to determine whether a delay in the start of the promoting regimen after the administration of a carcinogen would influence the promoting efficacy of orotic acid on the development of hepatocellular carcinoma in rats. Male Fischer 344 rats weighing 130-150 g were injected with a single dose of diethylnhrosamine (200 mg/kg body wt i.p.) then divided into 3 groups: groups 1 and 2 were given semi-synthetic basal diet or the same diet containing 1% orotic acid (OA) respectively starting 1 week after the carcinogen; group 3 received the OA diet starting 5 weeks after the administration of diethylnitrosamine. Animals from these 3 groups were sacrificed after 25, 32, 42 and 60 weeks of being fed their respective diets. The results indicated that delaying the start of the OA diet after the carcinogen resulted in about a 50% decrease in the incidence of hepatic nodules and/or hepatocellular carcinomas at various time points during the experiment. This decrease in promoting efficacy of OA was not apparently explainable by lack of metabolic effects of OA, at least in terms of induction of nucleotide pool imbalance, a condition that appears to be important for OA to exert its tumor promoting effects.