Abstract

Host intracellular iron has been recognized as an important cofactor in induction of nicotinamide adenine dinucleotide phosphate (NADPH)-dependent oxidative burst as antimicrobial defense mechanism. It is plausible that iron chelator directly inactivates NADPH oxidase by chelating the active site heme iron of flavocytochrome b558 thus blocking the transfer of electrons from NADPH to oxygen and its reduction to superoxide anion. Thus, altering the equilibrium of intracellular iron could influence the course of infection to the enhancement of the pathogen with regard to oxidative stress.

Keywords: Helicobacter pylori, NADPH, iron, free radicals, nicotinamide adenine dinucleotide phosphate, heme iron, flavocytochrome b558, iron chelator, gastritis appears, neutrophils, macrophages, Chronic gastritis, immunoglobulin-secreting plasma cells, reactive oxygen species, superoxide dismutase, Phagocytic leukocytes, Nox, NADPH-dependent oxidative burst, chemoattractants, chemokines, Phagocytic cytochrome b558, desferrioxamine, neutrophil-activating protein, monocyte-dependent fashion, mononuclear cell depletion, Ficoll-purified neutrophils, pentose phosphate pathway, nonoxidative pentose pathway, glucose-6-phosphate dehydrogenase, glutathione, glutathione metabolism, hydrogen peroxide, hepatocytes, hypoferremia, peptide hormone hepcidin, duodenal enterocytes, iron-recycling macrophages, iron-storing hepatocytes, erythropoiesis, ironbinding molecules, siderophores, Haber-Weiss reaction, iron deficiency anemia