“…Other enzyme systems that are potential sources for H 2 O 2 , including xanthine oxidase, cytochrome P-450, NO synthase, and cyclooxygenase-1, were less likely sources because their respective inhibitors, (allupurinol, cimetidine, L-NAME, and indomethacin) did not inhibit UPinduced H 2 O 2 release. The NAD(P)H oxidase activity in vascular endothelial cells can be stimulated by many plasma membranemediated events, including cytokines, hormones, growth factors, G protein receptor agonists, and shear forces, and activation of NAD(P)H oxidase is known to be involved in the pathogenesis of vascular disease (15,20,21,24,34). Electron leaks from the mitochondrial electron transport chain of vascular endothelial cells, on the other hand, have been observed with different stimuli, such as hypoxia-reoxygenation and glucocorticoid excess (28,43).…”