Inflammatory diseases of the respiratory tract are commonly associated with elevated production of nitric oxide (NO*) and increased indices of NO* -dependent oxidative stress. Although NO* is known to have anti-microbial, anti-inflammatory and anti-oxidant properties, various lines of evidence support the contribution of NO* to lung injury in several disease models. On the basis of biochemical evidence, it is often presumed that such NO* -dependent oxidations are due to the formation of the oxidant peroxynitrite, although alternative mechanisms involving the phagocyte-derived heme proteins myeloperoxidase and eosinophil peroxidase might be operative during conditions of inflammation. Because of the overwhelming literature on NO* generation and activities in the respiratory tract, it would be beyond the scope of this commentary to review this area comprehensively. Instead, it focuses on recent evidence and concepts of the presumed contribution of NO* to inflammatory diseases of the lung.