Linked Life Data

12935310

Source:http://linkedlifedata.com/resource/pubmed/id/12935310

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2003-8-25
pubmed:abstractText
The bioenergetic properties of mitochondria in combination with the high turnover rate of dioxygen qualify these organelles for the formation of reactive oxygen species (ROS). The assumption that mitochondria are the major intracellular source of ROS was essentially based on in vitro experiments with isolated mitochondria. The transfer of these data to the living cell may, however, be incorrect. Artefacts due to the preparation procedure or inadequate detection methods of ROS may lead to false positive results. Inhomogeneous results were found to be due to an interaction of the detection system with components of the respiratory chain which could be avoided by a recently developed non-invasive method. One of the most critical electron transfer steps in the respiratory chain is the electron bifurcation from ubiquinol to the cytochrome bc(1) complex. This electron bifurcation requires the free mobility of the head domain of the Rieske iron-sulfur protein. Inhibition of electron bifurcation by antimycin A causes leakage of single electrons to oxygen which results in the release of ROS. Hindrance of electron bifurcation was also observed following alterations of the physical state of membrane phospholipids in which the cytochrome bc(1) complex is inserted. Irrespective of whether the fluidity of the membrane was elevated or decreased, electron flow rates to the Rieske iron-sulfur protein were drastically reduced. Concomitantly superoxide radicals were released from these mitochondria, strongly suggesting the involvement of the ubiquinol/cytochrome bc(1) redox couple in this process.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1351-0002
pubmed:author
pubmed:issnType
Print
pubmed:volume
8
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
135-41
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Are mitochondria a spontaneous and permanent source of reactive oxygen species?
pubmed:affiliation
Fundamental Pharmacology and Toxicology, University of Veterinary Medicine Vienna, Vienna, Austria. hans.nohl@vu-wien.ac.at
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't