Linked Life Data

17115935

Source:http://linkedlifedata.com/resource/pubmed/id/17115935

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-5-3
pubmed:abstractText
Ca2+ overload of mitochondria and oxidants are considered as crucial factors inducing the opening of the permeability transition pore (PTP) in mitochondria. The interdependence between permeability transition (PT), calcium retention capacity (CRC), and reactive oxygen species (ROS) generation was studied in mitochondria from immature and mature rat brain. Brain mitochondria isolated from 1-day- and 1-week-old rats are much more resistant to Ca2+-triggered PT in phosphate-containing incubation medium than mitochondria from adult brain, since the CRC decreases with development. CRC of mitochondria from 1-week-old rat brain was higher than for adult rat brain (450 +/- 112 vs. 175 +/- 35 nmol Ca2+ per mg of protein). In contrast, for ROS generation there was no age difference. In immature and mature mitochondria, basal, respiratory chain-inhibited or glutathione-depleted ROS generations were similar. In addition, the extent of the Ca2+ load was without effect on the basal ROS generation before mitochondria underwent PT. In summary, ROS generation does not crucially affect the ability of immature mitochondria to buffer high levels of extramitochondrial Ca2+ without undergoing PT. However, we hypothesize that the high resistance of immature mitochondria is related to the low content of some PTP complex constituents, such as creatine kinase.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1523-0864
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
191-9
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Ca2+ storage capacity of rat brain mitochondria declines during the postnatal development without change in ROS production capacity.
pubmed:affiliation
Institut für Biochemie, Otto-von-Guericke-Universität Magdeburg, Germany. peter.Schoenfeld@medizin.uni-magdeburg.de
pubmed:publicationType
Journal Article