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SO release from leukocytes via NADPH oxidase activation contributes to oxidative stress under various diseases, such as ischemia/reperfusion (I/R) injury and vascular complications in diabetes. NADPH oxidase has seven isoforms with NOX2 being the predominant isoform of NADPH oxidase in polymorphonuclear leukocytes (PMNs). Activation of NOX2 requires the assembly of cytosolic subunits (p47, p40, p67, Rac) to plasma membrane subunits (gp91 and p22) [1]. NADPH oxidase is activated during I/R injury via cytokine receptor stimulation or chemotactic factor (N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP, MW= 438 g/mol) and utilizes molecular oxygen to produce SO [2] (Figure 1).

Comparing the Effectiveness of TAT and Myristoylation of gp91ds on Leukocyte Superoxide (SO) Release