Endothelial cell viability is maintained by a growth factor, vascular endothelial growth factor. This factor binds to a receptor, KDR, located on the surface of endothelial cells. This interaction ensures endothelial cell survival. Any interference with this pathway will lead to endothelial death, destruction of the alveoli, and emphysema. We believe that an increase in oxidative stress, rather than increased inflammation, is the trigger that results in this destruction. A drug which inhibits KDR and therefore interferes with growth factor function, produces emphysema after 3 weeks of administration to rats. Interestingly, this emphysema is in the absence of inflammatory cells, but in the presence of substantial oxidative stress. Protein oxidation was tested in the lungs of the drug treated rats by a method that specifically identifies target proteins. With this method, increased intensity of a band indicates increased oxidation. The results of such an experiment are shown below in Figure 1. The left panel shows proteins isolated from human lungs. The right panel shows lungs of rats exposed to the drug. The control (C) and the no emphysema lanes show decreased intensity of both MnSOD and KDR proteins. However, in the emphysematous and drug-treated rats, there is increased staining, suggesting increased oxidation of both of these proteins. Increased oxidation of SOD decreases its activity, while the effects of increased oxidation of KDR are not known.