Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6-7
pubmed:dateCreated
2001-1-11
pubmed:abstractText
Mitochondria are incompletely coupled, and during oxidative phosphorylation some of the redox energy in substrates is lost as heat. Incomplete coupling is mostly due to a natural leak of protons across the mitochondrial inner membrane. In rat hepatocytes the futile cycle of proton pumping and proton leak is responsible for 20-25% of respiration; in perfused rat muscle the value is 35-50%. Mitochondrial proton cycling is estimated to cause 20-25% of basal metabolic rate in rats. Proton cycling is equally prominent in hepatocytes from several different mammalian and ectotherm species, so it may be a general pathway of ecologically significant energy loss in all aerobes. Because it occurs in ectotherms, thermogenesis cannot be its primary function. Instead, an attractive candidate for the function of the universal and expensive energy-dissipating proton cycle is to decrease the production of superoxide and other reactive oxygen species (ROS). This could be important in helping to minimise oxidative damage to DNA and in slowing ageing. Mitochondria are the major source of cellular ROS, and increased mitochondrial proton conductance leads to oxidation of ubiquinone and decreased ROS production in isolated mitochondria. However, to date there is no direct evidence in cells or organisms that mitochondrial proton cycling lowers ROS production or oxidative damage or that it increases lifespan.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0531-5565
pubmed:author
pubmed:issnType
Print
pubmed:volume
35
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
811-20
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Uncoupling to survive? The role of mitochondrial inefficiency in ageing.
pubmed:affiliation
MRC Dunn Human Nutrition Unit, Hills Road, CB2 2XY, Cambridge, UK. martin.brand@mrc-dunn.cam.ac.uk
pubmed:publicationType
Journal Article, Review