Linked Life Data

17127357

Source:http://linkedlifedata.com/resource/pubmed/id/17127357

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2006-11-27
pubmed:abstractText
Nitric oxide (NO) and its derivatives (reactive nitrogen species) have multiple effects on mitochondria that impact on cell physiology and cell death. Mitochondria may produce and consume NO and NO stimulates mitochondrial biogenesis, apparently via cGMP upregulation of transcriptional factors. NO inhibits mitochondrial respiration via: (A) an acute and reversible inhibition of cytochrome oxidase by NO in competition with O2, and (B) irreversible inhibition of multiple sites by reactive nitrogen species. NO is a potent vasodilator (via cGMP), increasing O2 and respiratory substrate supply to mitochondria. NO stimulates reactive oxygen and nitrogen species production from mitochondria via respiratory inhibition, reaction with ubiquinol and reaction with O2 in the membrane. NO can induce apoptosis, mainly via oxidative stress. NO induces necrosis, mainly via energy depletion. Reactive nitrogen species activation of the mitochondrial permeability transition pore may cause apoptosis or necrosis. NO may protect against mitochondria-mediated cell death by multiple mechanisms.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1093-4715
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1024-33
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Nitric oxide and mitochondria.
pubmed:affiliation
Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, United Kingdom. gcb@mole.bio.cam.ac.uk
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't