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首页> 外文学位 >Lipoic Acid and its Potential Role in the Treatment of Oxidative-Induced Injury of A549 Lung Epithelial Cells.
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Lipoic Acid and its Potential Role in the Treatment of Oxidative-Induced Injury of A549 Lung Epithelial Cells.

机译：硫辛酸及其在A549肺上皮细胞氧化性损伤治疗中的潜在作用。

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摘要

Oxidative stress is the imbalance between prooxidants and antioxidants within a cell that can cause and/or contribute to the progression of many pathological conditions. Reactive oxygen species (ROS) formed from the metabolism of hydrogen peroxide (H2O2) or paraquat (PQ) can damage DNA, proteins, and polyunsaturated fatty acids (PUFAs). A cell's ability to defend against oxidative stress depends on multiple factors including genetic make-up, subcellular organelle function and environmental factors. Lipoic acid (LA) is an antioxidant with high reactivity to free radicals, but because of its low redox potential, it is also known to regenerate ascorbic acid and α-tocopherol, elevate intracellular glutathione (GSH) levels and modulate transcription factor activity. We used A549 lung epithelial cells in an in vitro model to study the mechanism(s) of LA effects against H2O2- and PQ-induced oxidative injury. We observed that LA was incapable of protecting against H2O2 toxicity; thus, we used PQ as the agent to induce oxidant-induced damage. Challenge of cells with PQ resulted in decreases of cell viability and mitochondrial membrane potential and increases in DNA fragmentation and intracellular Ca 2+ levels. Challenge of cells with LA resulted in an increase in cell viability, but a decrease in mitochondrial membrane potential. Interestingly, LA pretreatment of PQ-challenged cells resulted in the potentiation of DNA fragmentation and intracellular Ca2+ levels. Our results indicate that LA enhanced the PQ-induced oxidative injury in A549 lung epithelial cells, perhaps by acting as a prooxidant.
机译：氧化应激是细胞内前氧化剂和抗氧化剂之间的不平衡，可导致和/或促进许多病理状况的发展。过氧化氢（H 2 O 2 ）或百草枯（PQ）代谢形成的活性氧（ROS）可以破坏DNA，蛋白质和多不饱和脂肪酸（PUFA） ）。细胞抵抗氧化应激的能力取决于多种因素，包括遗传组成，亚细胞器功能和环境因素。硫辛酸（LA）是一种对自由基具有高反应活性的抗氧化剂，但由于其氧化还原电势较低，因此还可以再生抗坏血酸和α-生育酚，提高细胞内谷胱甘肽（GSH）的水平并调节转录因子的活性。我们在体外模型中使用了A549肺上皮细胞，研究了LA对H 2 O 2 -和PQ的作用机制引起的氧化损伤。我们观察到LA不能抵抗H 2 O 2 毒性；因此，我们使用PQ作为试剂来诱导氧化剂引起的损害。用PQ刺激细胞会降低细胞活力和线粒体膜电位，并增加DNA片段和细胞内Ca 2 + 的水平。用LA挑战细胞导致细胞活力增加，但线粒体膜电位降低。有趣的是，LA预处理PQ挑战的细胞可增强DNA片段化和细胞内Ca 2 + 的水平。我们的结果表明，LA可能通过充当前氧化剂来增强PQ诱导的A549肺上皮细胞的氧化损伤。

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  • 作者

    Pycko, Roxanne.;

  • 作者单位

    Lakehead University (Canada).;

  • 授予单位 Lakehead University (Canada).;
  • 学科 Biology General.;Biology Cell.
  • 学位 M.S.
  • 年度 2012
  • 页码 107 p.
  • 总页数 107
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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