作者: George Thomas , Tasuke Ando , Kiran Verma , Elliott Kagan
DOI: 10.1007/978-3-642-79041-6_11
关键词: Reactive oxygen species 、 Superoxide 、 Asbestos 、 Chemistry 、 Hydroxyl radical 、 Nitric oxide 、 Radical 、 Catalase 、 Molecular biology 、 Superoxide dismutase
摘要: It is well recognized that inhalation of asbestos fibers linked to the causation a variety clinical disorders including interstitial pulmonary fibrosis, parietal pleural plaques, bronchogenic carcinoma and diffuse malignant mesothelioma pleura peritoneum (Kagan, 1985; Mossman Gee, 1989). Although pathogenesis these diseases has not been elucidated fully, there evidence alveolar macrophages (AM) play pivotal role in mediating asbestos-related injury. Thus, studies asbestosexposed rodents workers have shown AM are recruited sites deposition inhaled 1988; Rom et al., 1991). also demonstrated fibres can activate secrete diverse group inflammatory mediators cytokine growth factors, chemoattractants arachidonic acid metabolites Rom, Several vitro phagocytic uptake generate reactive oxygen species (ROS) such as superoxide anion \((O_2^{* - })\), hydroxyl radical (OH*) hydrogen peroxide (Shull, 1992; Mossman, 1986). reported scavengers free radicals, dismutase (SOD) catalase, may ameliorate injurious effects exposure (Mossman, al,. 1986; 1990). These predicated on })\)-driven, iron-catalyzed, Fenton-Haber-Weiss reactions which OH* (Grisham, 1992), suggest ROS an important pathobiology disease.