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致癌物诱导的哺乳动物线粒体DNA链断裂。

Strand breaks of mammalian mitochondrial DNA induced by carcinogens.

作者信息

Miyaki M, Yatagai K, Ono T

出版信息

Chem Biol Interact. 1977 Jun;17(3):321-9. doi: 10.1016/0009-2797(77)90095-3.

Abstract

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 strand 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 by 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 the treatment of cells with carcinogens, recovered during post-treatment incubation.

摘要

通过将哺乳动物细胞暴露于致癌物N-甲基-N'-硝基-N-亚硝基胍(MNNG)和4-硝基喹啉-1-氧化物(4NQO),细胞中的闭环线粒体DNA被降解为开环形式。在相同浓度下,MNNG比4NQO引起更多的线粒体DNA链断裂。致癌物对线粒体DNA的作用与对核DNA的作用不平行,核DNA受4NQO的损伤比受MNNG的损伤更明显。细胞在处理后4至20小时的孵育过程中,致癌物损伤的线粒体DNA未得到修复。用致癌物处理细胞后,标记胸苷掺入闭环线粒体DNA的量减少,但在处理后的孵育过程中恢复。

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