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首页> 外文期刊>Journal of biochemical and molecular toxicology >Depletion of mitochondrial DNA and enzyme in estrogen-induced hamster kidney tumors: a rodent model of hormonal carcinogenesis.
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Depletion of mitochondrial DNA and enzyme in estrogen-induced hamster kidney tumors: a rodent model of hormonal carcinogenesis.

机译：雌激素诱导的仓鼠肾肿瘤中线粒体DNA和酶的消耗：激素致癌的啮齿动物模型。

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Mitochondrial DNA (mtDNA) encodes for 13 polypeptides critical for normal functioning of the electron transport chain and damage to mtDNA has been associated with aging, and implicated in several disease processes. Although damage to mtDNA is being implicated in mutagenesis and carcinogenesis, there are limited studies demonstrating the role and extent of mtDNA damage in human or rodent cancers. Using serial dilution and competitive polymerase chain reaction analysis, we have quantitated the amount of total mtDNA and analyzed the extent of mtDNA damage in estrogen-induced and estrogen-dependent hamster kidney tumors. The hamster kidney tumor model is a useful and widely investigated rodent model of hormonal carcinogenesis, which shares several characteristics with human breast and uterine cancers, and point to a common mechanistic pathway. Our data indicate a significant decrease in the copy number of total mtDNA and the activity of a nuclear-encoded mitochondrial enzyme citrate synthase in hamster kidney tumors compared to age-matched controls. Since there are several hundred mitochondria in a cell and each mitochondrion has multiple copies of mtDNA, a very small percentage of somatic deletion mutation may not be enough to result in a decreased capacity of the mitochondrial genome. However, a significant increase in deletion mutations or a decrease in the mtDNA copy number can result in a decreased oxidative phosphorylation capacity of the mitochondria and decreased energetics, and thus increased susceptibility to the disease process. Therefore, estrogen-induced hamster kidney tumor model can be a useful rodent model of carcinogenesis to understand the role of mtDNA damage in cancer progression and development. Copyright 2002 Wiley Periodicals, Inc. J Biochem Mol Toxicol 16:1-9, 2002; DOI 10.1002/jbt.10017
机译：线粒体DNA（mtDNA）编码13种对电子传输链的正常功能至关重要的多肽，并且对mtDNA的损害与衰老有关，并涉及多种疾病过程。尽管对mtDNA的破坏与诱变和致癌作用有关，但很少有研究表明mtDNA在人类或啮齿动物癌症中的作用和程度。使用连续稀释和竞争性聚合酶链反应分析，我们已经定量了总mtDNA的量，并分析了在雌激素诱导和依赖雌激素的仓鼠肾肿瘤中mtDNA的损伤程度。仓鼠肾脏肿瘤模型是一种有用且经过广泛研究的啮齿动物激素致癌模型，它与人乳腺癌和子宫癌具有多个特征，并指出了一种常见的机制途径。我们的数据表明与年龄匹配的对照组相比，仓鼠肾肿瘤中总mtDNA的拷贝数和核编码的线粒体酶柠檬酸合酶的活性显着降低。由于细胞中有数百个线粒体，并且每个线粒体均具有多个mtDNA拷贝，因此体细胞缺失突变的很小百分比可能不足以导致线粒体基因组容量降低。但是，缺失突变的显着增加或mtDNA拷贝数的减少会导致线粒体的氧化磷酸化能力降低和能量降低，从而增加对疾病过程的易感性。因此，雌激素诱导的仓鼠肾肿瘤模型可以作为有用的啮齿类动物癌变模型，以了解mtDNA损伤在癌症进展和发展中的作用。版权所有2002 Wiley Periodicals，Inc. J Biochem Mol Toxicol 16：1-9，2002; DOI 10.1002 / jbt.10017

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