School of Medicine Osijek, Department of Clinical Laboratory Diagnostic, Croatia.
Mini Rev Med Chem. 2010 Dec;10(14):1309-15. doi: 10.2174/138955710793564160.
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.
宿主细胞内的铁已被认为是诱导烟酰胺腺嘌呤二核苷酸磷酸（NADPH）依赖性氧化爆发的重要辅助因子，作为抗菌防御机制。铁螯合剂通过螯合 flavocytochrome b558 的活性位点血红素铁直接使 NADPH 氧化酶失活，从而阻止电子从 NADPH 向氧转移及其还原为超氧阴离子。因此，改变细胞内铁的平衡可能会影响感染的过程，使病原体更容易受到氧化应激的影响。
