The role of reactive oxygen and nitrogen species in cellular iron metabolism |
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Authors: | Mladenka Premysl Simůnek Tomás Hübl Mojmír Hrdina Radomír |
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Institution: | Department of Pharmacology and Toxicology, Faculty of Pharmacy in Hradec Králové, Charles University in Prague, Heyrovského 1203, 500 05 Hradec Králové, Czech Republic. mladenkap@faf.cuni.cz |
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Abstract: | The catalytic role of iron in the Haber-Weiss chemistry, which results in propagation of damaging reactive oxygen species (ROS), is well established. In this review, we attempt to summarize the recent evidence showing the reverse: That reactive oxygen and nitrogen species can significantly affect iron metabolism. Their interaction with iron-regulatory proteins (IRPs) seems to be one of the essential mechanisms of influencing iron homeostasis. Iron depletion is known to provoke normal iron uptake via IRPs, superoxide and hydrogen peroxide are supposed to cause unnecessary iron uptake by similar mechanism. Furthermore, ROS are able to release iron from iron-containing molecules. On the contrary, nitric oxide (NO) appears to be involved in cellular defense against the iron-mediated ROS generation probably mainly by inducing iron removal from cells. In addition, NO may attenuate the effect of superoxide by mutual reaction, although the reaction product—peroxynitrite—is capable to produce highly reactive hydroxyl radicals. |
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Keywords: | c-acon cytosolic aconitase NOS NO-synthase IFNγ interferon γ iNOS cytokine-inducible NOS IRE iron responsible element IRP1 IRP2 iron regulatory proteins 1 and 2 LPS lipopolysacharide m-acon mitochondrial aconitase Ser serin SNAP S-nitroso-N-acetyl-d l-penicilamine SOD superoxide dismutase ROS reactive oxygen species Tf-Fe2 iron loaded transferrin TfR1 transferrin receptor 1 TNF-α tumor necrosis factor α |
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