Consequences of the electrogenic function of the phagocytic NADPH oxidase

Balázs K. Rada, Miklós Geiszt, Csilla Hably, Erzsébet Ligeti

Research output: Contribution to journalArticle

22 Citations (Scopus)


NADPH 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 O2.- 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.

Original languageEnglish
Pages (from-to)2293-2300
Number of pages8
JournalPhilosophical Transactions of the Royal Society B: Biological Sciences
Issue number1464
Publication statusPublished - Dec 29 2005



  • (O) production
  • Bacterial killing
  • Chronic granulomatous disease
  • Intracellular Ca homeostasis
  • NADPH oxidase
  • Neutrophilic granulocytes

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Agricultural and Biological Sciences(all)

Cite this