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

The iron regulatory proteins: targets and modulators of free radical reactions and oxidative damage / G. Cairo, S. Recalcati, A. Pietrangelo, G. Minotti. - In: FREE RADICAL BIOLOGY & MEDICINE. - ISSN 0891-5849. - 32:12(2002), pp. 1237-1243.

The iron regulatory proteins: targets and modulators of free radical reactions and oxidative damage

G. Cairo
Primo
;
S. Recalcati
Secondo
;
A. Pietrangelo
Penultimo
;
2002

Abstract

Iron acquisition is a fundamental requirement for many aspects of life, but excess iron may result in formation of free radicals that damage cellular constituents. For this reason, the amount of iron within the cell is carefully regulated in order to provide an adequate level of a micronutrient while preventing its accumulation and toxicity. A major mechanism for the regulation of iron homeostasis relies on the post-transcriptional control of ferritin and transferrin receptor mRNAs, which are recognized by two cytoplasmic iron regulatory proteins (IRP-1 and IRP-2) that modulate their translation and stability, respectively. IRP-1 can function as a mRNA binding protein or as an aconitase, depending on whether it disassembles or assembles an iron-sulfur cluster in response to iron deficiency or abundancy, respectively. IRP-2 is structurally and functionally similar to IRP-1, but does not assemble a cluster nor exhibits aconitase activity. Here we briefly review the role of IRP in iron-mediated damage induced by oxygen radicals, nitrogen-centered reactive species, and xenobiotics of pharmacological and clinical interest.
Free radicals; Iron; Iron regulatory proteins; Nitric oxide; Oxygen radicals; Xenobiotics
Settore MED/04 - Patologia Generale
2002
Article (author)
File in questo prodotto:
File Dimensione Formato  
1-s2.0-S0891584902008250-main.pdf

accesso riservato

Tipologia: Publisher's version/PDF
Dimensione 94.04 kB
Formato Adobe PDF
94.04 kB Adobe PDF   Visualizza/Apri   Richiedi una copia
Pubblicazioni consigliate

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/431206
Citazioni
  • ???jsp.display-item.citation.pmc??? 34
  • Scopus 159
  • ???jsp.display-item.citation.isi??? 147
social impact