Endogenous hepatic growth-modulating factors and effects of a choline-devoid diet and of phenobarbital on hepatocarcinogenesis in the rat.
Endogenous hepatic growth-modulating factors and effects of a choline-devoid diet and of phenobarbital on hepatocarcinogenesis in the rat.
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内源性肝生长调节因子以及无胆碱饮食和苯巴比妥对大鼠肝癌发生的影响。
DOI：
10.1080/01635588509513849
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Reddy,TV
中科院分区：
文献类型：
--
作者：
Lombardi,B;Ove,P;Reddy,TV
在假手术（SO）或部分肝切除（PH）的成年大鼠肝脏中测定了一种内源性细胞增殖抑制剂和一种细胞增殖刺激剂的活性；给大鼠喂食胆碱补充（CS）或胆碱缺乏（CD）的饮食；同样的饮食，随后急性CCU中毒；在相同的饲粮中添加苯巴比妥（PHB）或含有DL -乙硫氨酸（ETH）的CD。抑制剂和刺激剂通过肝细胞质分数乙醇沉淀半纯化，并通过体外生物测定法评估其活性。SO大鼠和CS喂养的大鼠肝脏只含有抑制剂活性。在PH、CD饮食或CCU中毒后，抑制剂活性被抑制，同时出现刺激活性。因此，PH、CD饮食和CCU中毒会导致成年大鼠肝脏中类似的细胞（损失和再生）和体液稳态变化。我们提出，这些变化构成了机制的基本属性，即三种情况对大鼠肝癌发生的影响相似，特别是在CD饮食的情况下，因为它诱导的变化是慢性的而不是急性的。PHB，另一个化学性肝癌发生的启动子，既不影响抑制剂也不影响刺激剂的活性。因此，PHB的作用机制似乎与其他三种药物不同。ETH没有改变由普通CD饮食引起的生长调节因子平衡的变化。这种转变可能解释了CD饮食对致癌物诱导的卵形细胞增殖的显著刺激。这些结果的意义是在已知的影响的背景下讨论CD饮食和PHB对大鼠肝癌的发生。
The activities of an endogenous inhibitor and of a stimulator of cell proliferation were assayed in the livers of sham‐operated (SO) or partially hepatectomized (PH) adult rats; rats fed a choline‐supplemented (CS) or a choline‐devoid (CD) diet; the same diets followed by acute CCU intoxication; the same diets supplemented with phenobarbital (PHB) or a CD diet containing DL‐ethionine (ETH). The inhibitor and the stimulator were semipurified by fractional ethanol precipitation of a liver cytosolic fraction, and their activities were assessed by means of bioassays in vitro. The livers of SO rats and of rats fed the CS diet contained only inhibitor activity. Following PH, a CD diet, or CCU intoxication the inhibitor activity was suppressed, and there was a simultaneous appearance of a stimulator activity. Thus, PH, a CD diet, and CCU intoxication cause similar cellular (loss and regeneration) and humoral‐homeostatic changes in adult rat livers. We propose that these changes constitute a basic attribute of the mechanism whereby the three conditions affect similarly hepatocarcinogenesis in the rat, especially in the case of a CD diet, because the changes it induces are chronic rather than acute. PHB, another promoter of chemical hepatocarcinogenesis, affected neither the inhibitor nor the stimulator activity. Thus, PHB seems to be acting by a different mechanism than that of the other three agents. ETH did not modify the shift in the balance of the growth‐modulating factors induced by a plain CD diet. This shift may account for the marked stimulation of carcinogen‐induced oval cell proliferation exerted by a CD diet. The significance of these results is discussed in the context of known effects of a CD diet and of PHB on hepatocarcinogenesis in rats.
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重复部分肝切除术作为大鼠肝脏对亚硝胺致癌反应的促进刺激。
影响因子：
8.8
作者：
A. Pound;L. Mcguire
通讯作者：
L. Mcguire
实验性致癌作用中的抗脂肽缺乏
DOI：
--
发表时间：
1980
期刊：
影响因子：
--
作者：
A. E. Rogers;P. Newberne
通讯作者：
P. Newberne
假定的癌前肝细胞群、增生结节对某些肝癌物质的急性细胞毒性作用的抵抗力。
影响因子：
11.2
作者：
E. Farber;S. Parker;M. Gruenstein
通讯作者：
M. Gruenstein
实验性四氯化碳中毒中的肝脏再生。*
DOI：
10.3181/00379727-102-25357
发表时间：
1959
影响因子：
--
作者：
C. M. Leevy;R. Hollister;R. Schmid;R. Macdonald;C. S. Davidson
通讯作者：
C. S. Davidson
无胆碱饮食和苯巴比妥在促进致癌物治疗大鼠肝脏中γ-谷氨酰转肽酶阳性肝细胞病灶出现方面的协同作用。
影响因子：
11.2
作者：
Shinozuka,H;Lombardi,B
通讯作者：
Lombardi,B