STRAND BREAKS OF MAMMALIAN MITOCHONDRIAL-DNA INDUCED BY CARCINOGENS
STRAND BREAKS OF MAMMALIAN MITOCHONDRIAL-DNA INDUCED BY CARCINOGENS
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DOI：
10.1016/0009-2797(77)90095-3
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发表时间：
1977-01-01
影响因子：
5.1
通讯作者：
ONO, T
中科院分区：
文献类型：
--
作者：
MIYAKI, M;YATAGAI, K;ONO, T
用致癌物N-甲基-N“-硝基-N-亚硝基胍（MNNG）和4-硝基喹啉-1-氧化物（4 NQO）处理哺乳动物细胞，使细胞线粒体DNA的闭环结构降解为开环结构。在相同浓度下，MNNG比4 NQO引起更多的线粒体DNA断裂。致癌物对线粒体DNA的作用与核DNA的作用不平行，4 NQO对线粒体DNA的损伤比MNNG更明显。在4-20小时的细胞处理后孵育期间，致癌物损伤的线粒体DNA没有修复。掺入标记的胸苷到封闭的环状线粒体DNA，减少了治疗的细胞与致癌物质，恢复后处理孵育。
Closed circular mitochondrial DNA in mammalian cells was degradated to the open circular form by exposure of the cells to the carcinogens N-methyl-N''-nitro-N-nitrosoguanidine (MNNG) and 4-nitroquinoline 1-oxide (4NQO). MNNG caused more stand scission of mitochondrial DNA than 4NQO at the same concentration. The action of the carcinogens on mitochondrial DNA did not parallel that with nuclear DNA which was damaged by 4NQO more markedly than MNNG. Mitochondrial DNA damaged by carcinogens was not repaired during 4-20 h of post-treatment incubation of the cells. Incorporation of labeled thymidine into the closed circular mitochondrial DNA, decreased by treatment of cells with carcinogens, recovered during post-treatment incubation.