Itze L, Vesselinovitch S D, Rao K V, Hruban Z, Itzeová V
Physiol Bohemoslov. 1979;28(2):151-9.
The present report is a continuation of our previous studies on the biochemical mechanisms of carcinogenesis; studying the nature of interactions taking place between Ethylnitrosourea and DNA, RNA and protein of various stages of their synthetic activity. As a model system we chose partially hepatectomized mice live 36 hrs after surgery. Synthetic macromolecule activity in the remaining liver segment was determined by means of 3H-thymidine, 3H-uridine and 3H-leucine. We observed complete depression of DNA synthetic activity (immediately after Ethylnitrosourea administration it remained depressed almost through out the whole period of our observations) while protein synthetic activity was highly elevated. Qualitative changes of soluble proteins which were analyzed by isoelectric fractionation on 5% polyacrylamide after previous 3H- and 14C-leucine incorporation, could not be detected. Our biochemical data are correlated with histological studies and with the tumour incidence following the Ethylnitrosourea treatment of partially hepatectomized mice in the course of long-term experiments. The results provide guideline for further analysis, which should be modified according to the information concerning Ethylnitrosourea carcinogenesis induced 36 hours after partial hepatectmoy.
本报告是我们先前关于致癌作用生化机制研究的延续；研究了乙基亚硝基脲与处于合成活性不同阶段的DNA、RNA和蛋白质之间相互作用的性质。作为模型系统，我们选择了术后存活36小时的部分肝切除小鼠。通过3H-胸腺嘧啶核苷、3H-尿苷和3H-亮氨酸测定剩余肝段中的合成大分子活性。我们观察到DNA合成活性完全受到抑制（在给予乙基亚硝基脲后立即受到抑制，在我们整个观察期间几乎一直保持抑制状态），而蛋白质合成活性则高度升高。在用3H-和14C-亮氨酸掺入后，通过在5%聚丙烯酰胺上进行等电分级分离分析的可溶性蛋白质的定性变化未被检测到。我们的生化数据与组织学研究以及在长期实验过程中对部分肝切除小鼠进行乙基亚硝基脲处理后的肿瘤发生率相关。这些结果为进一步分析提供了指导方针，应根据部分肝切除术后36小时诱导的乙基亚硝基脲致癌作用的相关信息进行修改。
