作者: Yvonne M. W. Janssen , Cynthia R. Timblin , Christine L. Zanella , L. Albert Jimenez , Brooke T. Mossman
DOI: 10.1007/978-1-4615-5981-8_16
关键词: Gene expression 、 Programmed cell death 、 Cell 、 Cell biology 、 Gene 、 Immunology 、 Carcinogenesis 、 Biology 、 Inflammation 、 Immune system 、 Regulation of gene expression
摘要: Several environmental toxicants may cause cell injury and disease through pathways generating active oxygen species (AOS) and/or affecting the redox status of cells.1,2 Although biochemical generation AOS have been characterized for many agents, little is known about how agents affect gene expression in target cells or immune system. For pollutants, such as asbestos tobacco smoke, oxidant occurs by multiple including direct reactions catalyzed fibers components cigarette smoke indirect mechanisms involving interactions metabolism. Since organelles be affected regulation complex. In addition, a multiplicity genes activated specific types, which then act coordinately opposing fashions to phenotypic changes. Lastly, oxidant-generating proliferative effects at low concentrations3 cytotoxicity death high concentrations.1,2 Thus patterns governed dose-response relationships.