Zapisek W F, Cronin G M, Lyn-Cook B D, Poirier L A
Division of Nutritional Toxicology, National Center for Toxicological Research, Jefferson, AR 72079.
Carcinogenesis. 1992 Oct;13(10):1869-72. doi: 10.1093/carcin/13.10.1869.
This study examines proto-oncogene hypomethylation in rat livers during the early stages of hepatocarcinogenesis by dietary methyl deprivation in the presence and absence of initiation by diethylnitrosamine (DEN). Male weanling F344 rats were fed a complete diet, or a diet deficient in methionine and choline (MDD). Half the animals in each dietary group were given a single initiating dose of DEN (20 mg/kg). Animals from each of the treatment groups were killed at 1, 3, 8, 16 and 32 weeks, and hepatic DNA was isolated. This DNA was digested with the restriction enzymes MspI and HpaII to determine the extent of methylation of the CCGG sequences in c-Ha-ras, c-Ki-ras and c-fos proto-oncogenes. The results indicate that the administration of the MDD produced hypomethylation of these proto-oncogenes at all times investigated, independent of DEN initiation. The methylation changes in the c-Ha-ras gene increased in intensity throughout the experiment until at 32 weeks they were similar to the patterns seen in both neoplastic and preneoplastic livers of rats fed the deficient diet for 18 months. These results demonstrate that early, selective hypomethylation of some, but not all, CCGG sites occurs in rats undergoing hepatocarcinogenesis by dietary methyl deprivation.
本研究通过在存在和不存在二乙基亚硝胺(DEN)启动的情况下进行饮食性甲基剥夺,来检测大鼠肝癌发生早期肝脏中原癌基因的低甲基化情况。雄性断奶F344大鼠分别喂食完全饲料或蛋氨酸和胆碱缺乏的饲料(MDD)。每个饮食组中的一半动物给予单次启动剂量的DEN(20mg/kg)。在第1、3、8、16和32周处死每个治疗组的动物,并分离肝脏DNA。用限制性内切酶MspI和HpaII消化该DNA,以确定c-Ha-ras、c-Ki-ras和c-fos原癌基因中CCGG序列的甲基化程度。结果表明,在所有研究时间点,给予MDD均会导致这些原癌基因的低甲基化,与DEN启动无关。在整个实验过程中,c-Ha-ras基因的甲基化变化强度不断增加,直至32周时,其模式与喂食缺乏饲料18个月的大鼠的肿瘤性和癌前性肝脏中所见模式相似。这些结果表明,在通过饮食性甲基剥夺发生肝癌的大鼠中会出现一些(但不是全部)CCGG位点的早期选择性低甲基化。