Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2001-3-9
pubmed:abstractText
Mammalian tissues have large amounts of available ATP which are generated by oxidative phosphorylation in mitochondria. For the maintenance of the human body, a large amount of oxygen is required to regenerate these ATP molecules. A small fraction of the inspired oxygen is converted to superoxide radical and related metabolites even under physiological conditions. Most reactive oxygen species react rapidly with a variety of molecules thereby interfering with cellular functions and induce various diseases. Nitric oxide (NO) is an unstable gaseous radical with high affinity for various molecules, such as hemeproteins, thiols, and related radicals. NO easily penetrates through cell membrane/lipid bilayers, forms dissociable complexes with these molecules and modulates cellular metabolism and functions. Because NO has an extremely high affinity for the superoxide radical, the occurrence of the latter might decrease the biological function of NO. Thus, superoxide radicals in and around vascular endothelial cells play critical roles in the pathogenesis of hypertension and vasogenic tissue injury. Because NO also reacts with molecular oxygen, it rapidly loses its biological activity, particularly under ambient atmospheric conditions where the oxygen tension is unphysiologically high. Thus, biological functions of NO are determined by the local concentrations of molecular oxygen and superoxide radicals.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1071-5762
pubmed:author
pubmed:issnType
Print
pubmed:volume
33
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
757-70
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Cross-talk between NO and oxyradicals, a supersystem that regulates energy metabolism and survival of animals.
pubmed:affiliation
Department of Biochemistry & Molecular Pathology, Osaka City University Medical School, Osaka, Japan. inoue@med.osaka-cu.ac.jp
pubmed:publicationType
Journal Article, Review