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.

Department of Pharmacology and Toxicology Faculty of Pharmacy in Hradec Králové Charles University Prague Heyrovského 1203 500 05 Hradec Králové Czech Republic

Citace poskytuje Crossref.org

Cardioprotective effects of iron chelator HAPI and ROS-activated boronate prochelator BHAPI against catecholamine-induced oxidative cellular injury

Comparison of various iron chelators and prochelators as protective agents against cardiomyocyte oxidative injury

Iron is not involved in oxidative stress-mediated cytotoxicity of doxorubicin and bleomycin