Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2001-3-26
pubmed:abstractText
The generation of reactive oxygen species has been suggested to occur at increased rates during apoptosis, but the validity and significance of this remain contentious. In several key studies levels of reactive oxygen species have been monitored using the intracellular probe dichlorofluorescin (DCFH(2)), which undergoes oxidation to the fluorescent dichlorofluorescein (DCF). We report here that cytochrome c, which is released from mitochondria during cell death, is a potent catalyst of DCF formation. In a model system using xanthine oxidase to generate superoxide radicals, the rate of DCF formation was insensitive to changes in the rate of superoxide production over a 17-fold range, but extremely sensitive to nanomolar concentrations of cytochrome c. Thus we conclude that the DCF fluorescence observed in dying cells is a reflection of increased cytosolic cytochrome c. Moreover, we suggest that the suppression of DCF formation by the anti-apoptotic oncoprotein Bcl-2, which has been suggested to have antioxidant properties, can be explained on the basis of its prevention of mitochondrial cytochrome c release.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0006-291X
pubmed:author
pubmed:copyrightInfo
Copyright 2001 Academic Press.
pubmed:issnType
Print
pubmed:day
23
pubmed:volume
282
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
329-33
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Cytochrome C is a potent catalyst of dichlorofluorescin oxidation: implications for the role of reactive oxygen species in apoptosis.
pubmed:affiliation
Gray Laboratory Cancer Research Trust, Mount Vernon Hospital, Northwood, Middlesex, HA6 2JR, United Kingdom. burkitt@graylab.ac.uk
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't