Alteration of superoxide dismutase activity in tracheal epithelial cells by asbestos and inhibition of cytotoxicity by antioxidants.
Alteration of superoxide dismutase activity in tracheal epithelial cells by asbestos and inhibition of cytotoxicity by antioxidants.
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石棉改变气管上皮细胞中的超氧化物歧化酶活性，并通过抗氧化剂抑制细胞毒性。
DOI：
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发表时间：
1986
期刊：
影响因子：
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通讯作者：
M. Shatos
中科院分区：
文献类型：
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作者：
B. Mossman;J. Marsh;M. Shatos
我们在此报告了超氧化物歧化酶（超氧化物 (O2-.) 清除剂）以及甘露醇和二甲基硫脲（羟基自由基 (OH.) 清除剂）对仓鼠气管上皮细胞系中石棉诱导的细胞毒性的抑制作用。通过使用这些试剂，暴露于温石棉和青石棉长纤维（长度大于 10 微米）的培养物中的细胞损伤得到改善。相反，O2-、OH、H2O2 或 1O2（单线态氧）清除剂并不能防止短（小于或等于 2 微米）温石棉或玻璃纤维对上皮细胞的损伤。这些结果表明活性氧是长石棉纤维对呼吸道细胞损伤的介质。通过使用免疫细胞化学和生化技术，我们在体外的仓鼠气管支气管上皮细胞和肺泡巨噬细胞以及大鼠和人类呼吸道的组织学切片中检测到了相当数量的铜锌超氧化物歧化酶。在体外暴露于青石棉或温石棉几天的气管上皮细胞中，总内源性超氧化物歧化酶（铜锌和锰形式）的活性增加，但在未处理的细胞和暴露于相当量的玻璃纤维的细胞中没有变化。大鼠吸入石棉或将培养的细胞暴露于石棉后，观察到上皮细胞和肺泡巨噬细胞都突出有长纤维。石棉长纤维的不成功吞噬作用加上氧自由基的产生可能解释了长纤维在石棉相关呼吸道疾病中致病潜力的增加。
We report here the inhibition of asbestos-induced cytotoxicity in a hamster tracheal epithelial cell line by superoxide dismutase, a scavenger of superoxide (O2-.), and by mannitol and dimethylthiourea, scavengers of the hydroxyl radical (OH.). By using these agents, cell damage was ameliorated in cultures exposed to long (greater than 10 microns in length) fibers of chrysotile and crocidolite asbestos. In contrast, injury to epithelial cells by short (less than or equal to 2 microns) chrysotile or glass fibers was not prevented by scavengers of O2-., OH., H2O2 or 1O2 (singlet oxygen). These results implicate active oxygen species as mediators of injury by long asbestos fibers to cells of the respiratory tract. By using immunocytochemical and biochemical techniques, we detected appreciable amounts of copper-zinc superoxide dismutase in hamster tracheobronchial epithelial cells and alveolar macrophages in vitro and in histologic sections of rat and human respiratory tract. Activity of total endogenous superoxide dismutase (copper-zinc and manganese forms) increased in tracheal epithelial cells exposed for several days in vitro to either crocidolite or chrysotile asbestos but was unchanged in untreated cells and those exposed to comparable amounts of glass fibers. After inhalation of asbestos by rats, or exposure of cells in culture to asbestos, long fibers were observed protruding from both epithelial cells and alveolar macrophages. The unsuccessful phagocytosis of long fibers of asbestos coupled with generation of oxygen free radicals might explain the increased pathogenic potential of long fibers in asbestos-associated diseases of the respiratory tract.