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Consequences of the electrogenic function of the phagocytic NADPH oxidase Rada BK; Geiszt M; Hably C; Ligeti EPhilos Trans R Soc Lond B Biol Sci 2005[Dec]; 360 (1464): 2293-300NADPH oxidase of phagocytic cells transfers a single electron from intracellular NADPH to extracellular O2, producing superoxide (O.-2), the precursor to several other reactive oxygen species. The finding that a genetic defect of the enzyme causes chronic granulomatous disease (CGD), characterized by recurrent severe bacterial infections, linked O.-2 generation to destruction of potentially pathogenic micro-organisms. In this review, we focus on the consequences of the electrogenic functioning of NADPH oxidase. We show that enzyme activity depends on the possibilities for compensating charge movements. In resting neutrophils K+ conductance dominates, but upon activation the plasma membrane rapidly depolarizes beyond the opening threshold of voltage-gated H+ channels and H+ efflux becomes the major charge compensating factor. K+ release is likely to contribute to the killing of certain bacteria but complete elimination only occurs if O.-2 production can proceed at full capacity. Finally, the reversed membrane potential of activated neutrophils inhibits Ca2+ entry, thereby preventing overloading the cells with Ca2+. Absence of this limiting mechanism in CGD cells may contribute to the pathogenesis of the disease.|Bacteria/*immunology[MESH]|Calcium/metabolism[MESH]|Escherichia coli[MESH]|Granulomatous Disease, Chronic/immunology/metabolism/*physiopathology[MESH]|H(+)-K(+)-Exchanging ATPase/metabolism[MESH]|Humans[MESH]|Membrane Potentials/physiology[MESH]|NADPH Oxidases/*metabolism[MESH]|Neutrophils/metabolism[MESH]|Phagocytosis/immunology/*physiology[MESH]|Potassium/metabolism[MESH]|Staphylococcus aureus[MESH]|Superoxides/*metabolism[MESH] |
