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首页> 外文期刊>BioMed research international >Oxidative Stress Induces Mitochondrial DNA Damage and Cytotoxicity through Independent Mechanisms in Human Cancer Cells
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Oxidative Stress Induces Mitochondrial DNA Damage and Cytotoxicity through Independent Mechanisms in Human Cancer Cells

机译：氧化应激通过人癌细胞的独立机制诱导线粒体DNA损伤和细胞毒性

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摘要

Intrinsic oxidative stress through increased production of reactive oxygen species (ROS) is associated with carcinogenic transformation, cell toxicity, and DNA damage. Mitochondrial DNA (mtDNA) is a natural surrogate to oxidative DNA damage. MtDNA damage results in the loss of its supercoiled structure and is readily detectable using a novel, supercoiling-sensitive real-time PCR method. Our studies have demonstrated that mtDNA damage, as measured by DNA strand breaks and copy number depletion, is very sensitive to exogenous H2O2 but independent of endogenous ROS production in both prostate cancer and normal cells. In contrast, aggressive prostate cancer cells exhibit a more than 10-fold sensitivity to H2O2-induced cell toxicity than normal cells, and a cascade of secondary ROS production is a critical determinant to the differential response. We propose a new paradigm to account for different mechanisms governing cellular oxidative stress, cell toxicity, and DNA damage with important ramifications in devising new techniques and strategies in prostate cancer prevention and treatment.
机译：通过增加反应性氧物质（ROS）产生的固有氧化应激与致癌转化，细胞毒性和DNA损伤有关。线粒体DNA（MTDNA）是氧化DNA损伤的天然替代。 MTDNA损伤导致其超级镀锡结构的损失，并且使用新颖的超级概念敏感的实时PCR方法易于检测。我们的研究表明，通过DNA链中断和拷贝数耗竭测量的MTDNA损伤对外源H2O2非常敏感，但与前列腺癌和正常细胞中的内源性ROS产生无关。相反，侵袭性前列腺癌细胞对H 2 O 2诱导的细胞毒性具有超过10倍的敏感性而不是正常细胞，并且级联ROS产生是对差分反应的关键决定因素。我们提出了一种新的范例，以考虑治疗细胞氧化应激，细胞毒性和DNA损伤的不同机制，并在推动前列腺癌预防和治疗中的新技术和策略方面具有重要的影响。

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