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在二乙基亚硝胺(DENA)诱发大鼠肝癌过程中,无论在E.Coli RNA聚合酶或大鼠肝RNA聚合酶Ⅱ作用下,肝染色质的体外转录活性都比正常大鼠的高,并有随肝脏恶化程度而增高的趋势。进一步研究证明在RNA聚合酶Ⅱ作用下,喂DENA大鼠肝染色质的转录起始点数量比正常肝的多;而在E.Coli RNA聚合酶作用下,两种染色质的转录起始点数量未见明显差异,但喂DENA大鼠的肝染色质转录的RNA链较长。癌变过程中,肝染色质组蛋白及非组蛋白含量都无明显改变,而RNA含量则较正常肝略有增高。
In the course of DENA-induced hepatocellular carcinoma, the hepatic chromatin had higher in vitro transcriptional activity than that of normal rats, both in E. coli RNA polymerase and rat liver RNA polymerase II , And with the degree of liver deterioration increased trend. Further studies showed that under the action of RNA polymerase Ⅱ, the number of transcriptional start points of hepatic chromatin in DENA-fed rats was more than that in normal liver; while in E. coli RNA polymerase, the number of transcriptional start points of both chromatin See significant differences, but the mRNA chain of hepatic chromatin transcribed in DENA-fed rats is longer. During carcinogenesis, there was no significant change in hepatic chromatin histone and non-histone content, while RNA content was slightly higher than normal liver.