Long-term exposure to sodium arsenite was found to induce malignant transformation in human bronchial epithelial (HBE) cell line as evidenced by elevated ROS levels. Although chronic sodium arsenite-induced HBE cell line transformation was associated with elevated ROS generation, it was of interest to determine whether acute sodium arsenite exposure also initiated pulmonary damage. Thus, the aim of this study was to investigate oxidative-stress-related pulmonary damage using a human bronchial epithelial (HBE) cell line. Incubation of ρ+-HBE (in the presence of mitochondrial DNA) cells with various concentrations of sodium arsenite, significantly increased ROS and MDA levels accompanied by decreased SOD activity in a concentration-dependent manner. In contrast, treatment of ρ-HBE (without mitochondrial DNA) cells various concentrations of sodium arsenite a reduction in ROS and MDA levels were noted. However, the SOD activity remained decreased in ρ-HBE cells. This was accompanied by a significant rise in HO-1 protein expressions levels in both cell types with greater changes ρ-HBE cells at the lower sodium arsenite concentrations. Data indicate that acute sodium arsenite exposure exerted a greater effect ρ-HBE cells suggesting that absence of mitochondrial DNA appears to enhance sensitivity to the oxidant actions of inorganic As.

中文翻译：

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线粒体DNA在亚砷酸钠诱导的人支气管上皮细胞氧化损伤中的作用。

发现长期暴露于亚砷酸钠可诱导人支气管上皮（HBE）细胞系发生恶性转化，如ROS水平升高所证明。尽管慢性亚砷酸钠诱导的HBE细胞系转化与ROS生成升高有关，但确定急性亚砷酸钠暴露是否也引起肺损伤仍很有意义。因此，本研究的目的是研究使用人类支气管上皮细胞（HBE）的氧化应激相关性肺损伤。用各种浓度的亚砷酸钠孵育ρ+ -HBE（存在线粒体DNA）细胞时，ROS和MDA含量显着增加，同时SOD活性以浓度依赖性方式降低。相反，注意到ρ-HBE（无线粒体DNA）细胞的处理各种浓度的亚砷酸钠可降低ROS和MDA水平。然而，在ρ-HBE细胞中SOD活性仍然降低。这伴随着两种细胞类型中HO-1蛋白表达水平的显着提高，而在较低的亚砷酸钠浓度下ρ-HBE细胞的变化更大。数据表明，亚砷酸钠的急性暴露对ρ-HBE细胞产生更大的影响，表明线粒体DNA的缺乏似乎增强了对无机As氧化作用的敏感性。这伴随着两种细胞类型中HO-1蛋白表达水平的显着提高，而在较低的亚砷酸钠浓度下ρ-HBE细胞的变化更大。数据表明，亚砷酸钠的急性暴露对ρ-HBE细胞产生更大的影响，表明线粒体DNA的缺乏似乎增强了对无机As氧化作用的敏感性。这伴随着两种细胞类型中HO-1蛋白表达水平的显着提高，而在较低的亚砷酸钠浓度下ρ-HBE细胞的变化更大。数据表明，亚砷酸钠的急性暴露对ρ-HBE细胞产生更大的影响，表明线粒体DNA的缺乏似乎增强了对无机As氧化作用的敏感性。