A Study on Mechanism for Development and Progression of Metal-related Lung Disease

接触钴和镍会导致肺炎、肺纤维化、哮喘和肺癌。在气管内灌注超细钴或镍，建立大鼠肺炎致肺纤维化模型。在大鼠肺急性炎症阶段，活性氧（ROS）和肿瘤坏死因子- α (tumor necrosis factor- α)参与其中。DNA质粒测定显示钴和镍具有致癌潜力。与细胞凋亡相关的Bcl-2蛋白也有表达。综上所述，这些发现表明，钴或镍的肺毒性会产生损伤DNA的活性氧，而活性氧的产生会诱导tnt - α的产生。细胞凋亡在金属相关性肺部疾病中的作用有待进一步研究。

Exposure to cobalt and nickel cause pneumonitis, pulmonary fibrosis, asthma and lung cancer. The model for pneumonitis resulting in pulmonary fibrosis was developed in the rat with tracheal instillation of ultrafine cobalt or nickel. At the stage of acute inflammation in the rat lungs reactive oxygen species (ROS) and tumor necrosis factor-alpha were involved. DNA plasmid assay showed carcinogenic potential of both cobalt and nickel. Bcl-2 protein related to apoptosis was also found to express. Taken together, these finding suggest that lung toxicity of cobalt or nickel generate ROS which damage DNA, and that the generation of ROS induce production of TNT-alpha. Further studies are needed on the role of apoptosis in metal-related lung diseases.