Linked Life Data

10443935

Source:http://linkedlifedata.com/resource/pubmed/id/10443935

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1999-11-12
pubmed:abstractText
Isolated mitochondria are well-established sources of oxidants in vitro. There is little direct evidence that mitochondria promote oxidative stress in vivo, however. Model system studies demonstrate that ortho-tyrosine, meta-tyrosine, and o,o'-dityrosine increase in proteins oxidized by hydroxyl radical. To determine whether mitochondria generate oxidants in vivo, we used isotope dilution gas chromatography mass spectrometry to quantify levels of these markers in the heart muscle of control and exercised rats. Exercise led to a 50% increase in ortho-tyrosine, metatyrosine, and o,o'-dityrosine in the mitochondrial proteins but not cytosolic proteins of heart muscle. This increase was transient, and levels returned to normal when exercised animals were allowed to rest. There also was a transient increase in the level of o,o'-dityrosine in the urine of exercised rats. This relationship between mitochondrial and urine levels of o,o'-dityrosine suggests that urine assays of this oxidized amino acid may serve as noninvasive measures of oxidative stress. These observations also provide direct evidence that heart muscle mitochondria produce an intermediate resembling the hydroxyl radical that promotes protein oxidation in vivo.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0891-5849
pubmed:author
pubmed:issnType
Print
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
186-92
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Hydroxyl radical generation during exercise increases mitochondrial protein oxidation and levels of urinary dityrosine.
pubmed:affiliation
Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't