Neutrophils are the host's first line of defense against many pathogenic bacteria and fungi. Their ability to kill invading microorganisms depends to a large extent on the respiratory burst, a sequence of events whereby the activated phagocyte reduces molecular oxygento a variety of toxic products. This dramaticincreaseinoxidativemetabolismtriggeredbyphagocytosis or exposure to certain inflammatory mediators is also characteristicofmononuclearphagocytesandeosinophilsbut is best understood in neutrophils. The initial product of the respiratory burst is the superoxide anion (OJ), whereas subsequent reactions lead to the formation of other toxic agents including hydrogen peroxide (H202), hypochlorous acid (HOCl) and possibly hydroxylradical (OH·) and singlet oxygen (102). The biochemical basis for the neutrophil respiratory burst has been under intensive study and the features of the rapidly emerging, though still incomplete, picture of the responsible oxidase are reviewed here (also see [1-5].