Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2003-11-25
pubmed:abstractText
The trace amounts of "free" iron can catalyse production of a highly toxic hydroxyl radical via Fenton/Haber-Weiss reaction cycle. The critical factor appears to be the availability and abundance of cellular labile iron pool (LIP) that constitutes a crossroad of metabolic pathways of iron-containing compounds and is midway between the cellular need of iron, its uptake and storage. To avoid an excess of harmful "free" iron, the LIP is kept at the lowest sufficient level by transcriptional and posttranscriptional control of the expression of principal proteins involved in iron homeostasis. The putative sources of cellular LIP, its homeostasis and its role in the cellular response to oxidative stress are discussed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0027-5107
pubmed:author
pubmed:issnType
Print
pubmed:day
29
pubmed:volume
531
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
81-92
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Labile iron pool: the main determinant of cellular response to oxidative stress.
pubmed:affiliation
Department of Radiobiology and Health Protection, Institute of Nuclear Chemistry and Technology, Dorodna 16, 03-195 Warsaw, Poland. marcinkr@orange.ichtj.waw.pl
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't