The role of reactive oxygen and nitrogen species in cellular iron metabolism
Language English Country England, Great Britain Media print
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
PubMed
16484042
DOI
10.1080/10715760500511484
PII: P1267205P1519467
Knihovny.cz E-resources
- MeSH
- Humans MeSH
- Iron-Sulfur Proteins metabolism MeSH
- Reactive Nitrogen Species metabolism MeSH
- Reactive Oxygen Species metabolism MeSH
- Iron metabolism MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- Iron-Sulfur Proteins MeSH
- Reactive Nitrogen Species MeSH
- Reactive Oxygen Species MeSH
- Iron MeSH
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.
References provided by Crossref.org
Iron is not involved in oxidative stress-mediated cytotoxicity of doxorubicin and bleomycin
