Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-6-8
pubmed:abstractText
Three distinct antioxidant pathways are considered through which iron-catalyzed oxidative stress may be regulated by nitric oxide (NO). The first two pathways involve direct redox interactions of NO with iron catalytic sites and represent a fast response that may be considered an emergency mechanism to protect cells from the consequences of acute and intensive oxidative stress. These are (i) NO-induced nitrosylation at heme and non-heme iron catalytic sites that is capable of directly reducing oxoferryl-associated radicals, (ii) formation of nitrosyl complexes with intracellular "loosely" bound redox-active iron, and (iii) an indirect regulatory pathway that may function as an adaptive mechanism that becomes operational upon long-term exposure of cells to NO. In the latter pathway, NO down-regulates expression of iron-containing proteins to prevent their catalytic prooxidant reactions.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1523-0864
pubmed:author
pubmed:issnType
Print
pubmed:volume
3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
189-202
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Antioxidant mechanisms of nitric oxide against iron-catalyzed oxidative stress in cells.
pubmed:affiliation
Department of Environmental and Occupational Health, University of Pittsburgh, PA 15238, USA. kagan@pitt.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review