Abstract
Pulmonary cells are both critical sources and targets of toxic reactive species, with the mechanisms of free radical formation and tissue target reactions poorly understood. NO can contribute to novel pathophysiologic reactions that can occur in lungs. The toxicology of inhaled .NO is poorly and incompletely described, and there is a limited mechanistic understanding of the significant contribution of .NO and O2.- to pulmonary pathologic conditions. Finally, antioxidant defense supplementation will be the most effective when the location and nature of toxic species contributing to tissue injury are revealed, and the antioxidants are site-directed.