The iron regulatory proteins: targets and modulators of free radical reactions and oxidative damage1,2 1Guest Editor: Mario Comporti 2This article is part of a series of reviews on “Iron and Cellular Redox Status.” The full list of papers may be found on the homepage of the journal.

摘要: Iron acquisition is a fundamental requirement for many aspects of life, but excess iron may result in formation free radicals that damage cellular constituents. For this reason, the amount within cell carefully regulated order to provide an adequate level micronutrient while preventing its accumulation and toxicity. A major mechanism regulation homeostasis relies on post-transcriptional control ferritin transferrin receptor mRNAs, which are recognized by two cytoplasmic regulatory proteins (IRP-1 IRP-2) modulate their translation stability, respectively. IRP-1 can function as mRNA binding protein or aconitase, depending whether it disassembles assembles iron-sulfur cluster response deficiency abundancy, IRP-2 structurally functionally similar IRP-1, does not assemble nor exhibits aconitase activity. Here we briefly review role IRP iron-mediated induced oxygen radicals, nitrogen-centered reactive species, xenobiotics pharmacological clinical interest.