作者: Sonia Scarfì , Umberto Benatti , Marina Pozzolini , Emanuela Clavarino , Chiara Ferraris
DOI: 10.1111/J.1742-4658.2006.05564.X
关键词:
摘要: Exposure to quartz particles induces a pathological process named silicosis. Alveolar macrophages initiate the disease through their activation, which is origin of later dysfunctions. Ascorbic acid known selectively dissolve surface. During reaction, ascorbic progressively disappears and hydroxyl radicals are generated from These observations may be relevant mammalian toxicity, as substantial amounts present in lung epithelium. We studied inflammatory response murine macrophage cell line RAW 264.7 incubated with acid-treated quartz, expression activity enzyme cyclo-oxygenase-2 (COX-2). COX-2 prostaglandin secretion were enhanced cells quartz. In contrast, no changes observed Aerosil OX50, an amorphous form silica. Quantification mRNA showed threefold increase compared controls. The transcription factors, NF-κB, pCREB AP-1, all implicated increased response. Reactive oxygen species (H2O2 OH•) involved this experimental model. Parallel experiments performed on rat alveolar bronchoalveolar lavage confirmed untreated conclusion, selective interaction with, modification of, by crucial event determining macrophages, subsequently develop into acute inflammation, eventually leading chronic pulmonary