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首页> 外文学位 >Mitochondrial energy and antioxidant system alterations in cells harboring mitochondrial DNA depletion: Implications in pathologies exhibiting mitochondrial dysfunction.
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Mitochondrial energy and antioxidant system alterations in cells harboring mitochondrial DNA depletion: Implications in pathologies exhibiting mitochondrial dysfunction.

机译：线粒体DNA耗竭的细胞中线粒体能量和抗氧化系统的改变：表现出线粒体功能障碍的病理学意义。

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摘要

For a long time it was assumed that mitochondria were highly efficient energy factories for the cell. However, to the contrary, it has been conclusively demonstrated that, other than being major producers of ATP in the cell, they generate superoxide (O2·-) as a byproduct of the respiratory chain. In neurodegenereative diseases, stroke or ischemic injury, and exposure to mitochondrial toxins, reactive species can overwhelm the cellular antioxidant defenses and induce oxidative stress. Oxidative stress can induce mitochondrial DNA (mtDNA) damage, lipid peroxidation, and structural alterations of important proteins. Such changes result in mitochondrial bioenergetic restriction and can induce cell death pathways. Tissues with high energy requirements such as brain, cardiac and skeletal muscles are particularly vulnerable to such assaults that create a devastating and vicious cycle of reactive oxygen species (ROS) production and macromolecule damage. There is a concerted effort to understand mitochondrial energy metabolism and maintenance. A clear understanding of such processes may be useful in developing biomarkers for mitochondrial dysfunction, and identify novel pharmacological or biological targets for various interventions to restore mitochondrial integrity in diseases. To this end, we have studied metabolic and antioxidant protein alterations in a U87 cell line challenged with mtDNA depletion. Since mtDNA damage or deletion is noted in aging brain, neurodegenerative diseases, mitochondrial myopathies, and nucleoside analogue-based HIV therapy, we hypothesized that such cell culture models can be invaluable in molecular studies that may have important diagnostic and clinical implications and applications.
机译：长期以来，人们一直认为线粒体是细胞的高效能源工厂。然而，相反地，已经有结论性地证明，除了作为细胞中ATP的主要产生者之外，它们还产生超氧化物（O2·-）作为呼吸链的副产物。在神经退行性疾病，中风或缺血性损伤以及接触线粒体毒素的情况下，反应性物种可能会使细胞的抗氧化防御能力不堪重负，并诱发氧化应激。氧化应激可诱导线粒体DNA（mtDNA）损伤，脂质过氧化和重要蛋白质的结构改变。此类变化导致线粒体生物能受限，并可以诱导细胞死亡途径。具有高能量需求的组织（例如大脑，心脏和骨骼肌）特别容易受到此类攻击的破坏，这些攻击会造成破坏性的恶性循环，破坏活性氧（ROS）的产生并破坏大分子。人们齐心协力了解线粒体能量的代谢和维持。对此类过程的清楚了解可能有助于开发线粒体功能障碍的生物标记物，并为各种干预措施确定新的药理或生物学靶标，以恢复疾病中的线粒体完整性。为此，我们已经研究了受mtDNA消耗挑战的U87细胞系中的代谢和抗氧化蛋白改变。由于在衰老的大脑，神经退行性疾病，线粒体肌病和基于核苷类似物的HIV治疗中发现了mtDNA的损伤或缺失，因此我们假设这种细胞培养模型在分子研究中具有重要的诊断和临床应用价值。

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  • 作者

    Isaac, Alfred Orina.;

  • 作者单位

    Idaho State University.;

  • 授予单位 Idaho State University.;
  • 学科 Biology Neuroscience.; Health Sciences Toxicology.; Health Sciences Pharmacology.
  • 学位 Ph.D.
  • 年度 2007
  • 页码 170 p.
  • 总页数 170
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 神经科学;毒物学（毒理学）;药理学;
  • 关键词

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