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[N-甲基-N'-硝基-N-亚硝基胍诱导致癌的大鼠胃黏膜中染色质超分子结构变化及胃蛋白酶原合成]

[Changes in the supramolecular structure of chromatin and pepsinogen synthesis in the gastric mucosa of rats undergoing N-methyl-N'-nitro-N-nitrosoguanidine-induced carcinogenesis].

作者信息

Kalinovskiĭ V P, Seĭts I F

出版信息

Eksp Onkol. 1986;8(1):32-5.

PMID:3948755
Abstract

A model of gastric tumour induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in rats made it possible to detect essential alterations of chromatin-DNA-protein complexes, that is a weakening of the DNA-protein linkage. The changes appear at early stages of carcinogenesis and persist in induced adenocarcinomas of the stomach. Simultaneously an inhibition was established in pepsinogen synthesis during MNNG carcinogenesis, which reflects a damage in expression of functionally important genetic information. This fact shows a molecular-genetic connection between the process of the gastric mucosa malignization and a disturbance of physiologically important tissue-specific gene functions.

摘要

用N-甲基-N'-硝基-N-亚硝基胍(MNNG)诱导大鼠产生胃肿瘤的模型,使得检测染色质-DNA-蛋白质复合物的本质改变成为可能,即DNA-蛋白质连接的减弱。这些变化出现在致癌作用的早期阶段,并在诱导产生的胃腺癌中持续存在。同时,在MNNG致癌过程中,胃蛋白酶原合成受到抑制,这反映了功能上重要的遗传信息表达受到损害。这一事实表明胃黏膜恶性化过程与生理上重要的组织特异性基因功能紊乱之间存在分子遗传学联系。

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