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Role of Nitric Oxide in the Progression of Pneumoconiosis

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Abstract

Conflicting evidence has been reported as to whether nitric oxide (NO) possesses anti-inflammatory or inflammatory properties. Data are presented indicating thatin vitro orin vivo exposure to selected occupational dusts, i.e., crystalline silica, organic dust contaminated with endotoxin, or asbestos, results in upregulation of inducible nitric oxide synthase (iNOS) and the production of NO by alveolar macrophages and pulmonary epithelial cells. Nitric oxide production is associated temporally and anatomically with pulmonary damage, inflammation, and disease progression in response to occupational dusts. Blockage of inducible nitric oxide synthase by administration of NOS inhibitors or in iNOS knockout mice decreases the magnitude of injury and inflammation followingin vivo exposure to silica, endotoxin, or asbestos. Therefore, NO may play an important role in the initiation and progression of pneumoconiosis.

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  1. Health Effects Laboratory Division, National Institute for Occupational Safety and Health, 1095 Willowdale Road, Morgantown, West Virginia, 26505, USA

    V. Castranova

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Castranova, V. Role of Nitric Oxide in the Progression of Pneumoconiosis. Biochemistry (Moscow) 69, 32–37 (2004). https://doi.org/10.1023/B:BIRY.0000016348.34175.53

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  • DOI: https://doi.org/10.1023/B:BIRY.0000016348.34175.53

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