期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 40, 期 4, 页码 601-607出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2005.09.030
关键词
asbestos; extracellular superoxide dismutase; pulmonary fibrosis; oxidative stress; nitrotyrosine; free radical
资金
- NHLBI NIH HHS [R01 HL063700-06, R01 HL063700, HL63700] Funding Source: Medline
- NIEHS NIH HHS [1F30ES01362] Funding Source: Medline
Asbestosis is a chronic form of interstitial lung disease characterized by inflammation and fibrosis that results from the inhalation of asbestos fibers. Although the pathogenesis of asbestosis is poorly understood, reactive oxygen species may mediate the progression of this disease. The antioxidant enzyme extracellular superoxide dismutase (EC-SOD) can protect the lung against a variety of insults; however, its role in asbestosis is unknown. To determine if EC-SOD plays a direct role in protecting the lung from asbestos-induced injury, intratracheal injections of crocidolite were given to wild-type and ec-sod-null mice. Bronchoalveolar lavage fluid (BALF) from asbestos-treated ec-sod-null mice at 24 h 14 days, or 28 days posttreatment showed increased inflammation and total BALF protein content compared to that of wild-type mice. In addition, lungs from ec-sod-null mice showed increased hydroxyproline content compared to those of wild-type mice, indicating a greater fibrotic response. Finally, lungs from ec-sod-null mice showed greater oxidative damage, as assessed by nitrotyrosine content compared to those of their wild-type counterparts. These results indicate that depletion of EC-SOD from the lung increases oxidative stress and injury in response to asbestos. (c) 2005 Elsevier Inc. All rights reserved.
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