论文部分内容阅读
目的：研究限量饮食（ＤＲ）对小鼠肝代谢活化致癌物以及致癌物导致的ＤＮＡ链断裂程度的影响。方法：用３２Ｐ后标记和高效液相色谱法测定致癌物ＤＮＡ主要加合物生成量；用随机寡核甘酸引物合成法（ＲＯＰＳ）测定ＤＮＡ链断裂程度；用体外代谢酶活性测定法检测有关代谢酶的活性。结果：①限量饮食减少小鼠肝中黄曲霉毒素Ｂ１（ＡＦＢ１）和２乙基氨基芴（２ＡＡＦ）ＤＮＡ加合物（ＡＦＣ８ｄＧ）的生成，同时也减少致癌物导致的ＤＮＡ链断裂；限量饮食增加苯并［ａ］芘（ＢａＰ）ＤＮＡ加合物（ＢａＰＮ２ｄＧ）和６硝基苯甲萘（６ＮＣ）ＤＮＡ总加合物的生成，也增加致癌物导致的ＤＮＡ链断裂。②在小鼠肝中，致癌物ＤＮＡ加合物的生成量与致癌物导致的ＤＮＡ链断裂程度密切相关；③限量饮食诱导某些与致癌物代谢有关的酶。结论：限量饮食特异地改变小鼠肝代谢酶的活性继而影响致癌物的代谢活化，这种作用在致癌过程的起始阶段可能起着重要的作用。
OBJECTIVE: To investigate the effect of dietary restriction (DR) on the extent of DNA strand breaks caused by liver metabolism-induced carcinogens and carcinogens in mice. Methods: 32Ppost labeling and high performance liquid chromatography were used to determine the amount of carcinogenDNA major adducts; DNA fragmentation was measured by random oligonucleotide primers (ROPS); and in vitro metabolic enzyme activity assay About metabolic enzyme activity. RESULTS: (1) Limited diet decreased the production of aflatoxin B1 (AFB1) and 2-AAF DNA adducts (AF-C8-dG) in mice liver, and also reduced carcinogens The resulting DNA strand breaks; limited diet increased benzo[a]pyrene (BaP)-DNA adducts (BaP-N2dG) and 6nitrobenzonaphthalene (6NC)DNA total adducts Generation also increases DNA strand breaks caused by carcinogens. 2 In the liver of mice, the amount of carcinogen-DNA adduct produced is closely related to the degree of DNA strand break caused by carcinogens; 3 Diets in certain limits induce certain enzymes involved in the metabolism of carcinogens. CONCLUSIONS: Limited diets specifically alter the activity of liver metabolic enzymes in mice and subsequently affect the metabolic activation of carcinogens, which may play an important role in the initial stages of carcinogenesis.