Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
30
pubmed:dateCreated
1993-12-1
pubmed:abstractText
In our preceding paper, we reported that a temperature-sensitive Chinese hamster ovary cell mutant, PGS-S, with thermolabile phosphatidylglycerophosphate synthase was defective in the biogenesis of both phosphatidylglycerol and cardiolipin (CL) at a nonpermissive temperature (Ohtsuka, T., Nishijima, M., and Akamatsu, Y. (1993) J. Biol. Chem. 268, 22908-22913). To investigate the biological role of cardiolipin, we examined the structure and function of mitochondria in mutant PGS-S cells, since CL is primarily found in the mitochondrial membranes of eukaryotic cells. Under conditions where the formation of CL was impaired, this mutant had both morphological and functional mitochondrial abnormalities, manifested by more stringent temperature sensitivity for cell growth in glucose-deficient medium and by reduced ATP production, increased glycolysis, and reduced oxygen consumption in intact cells. Rotenone-sensitive NADH oxidase activity in cell extracts was also reduced in the mutant cultivated at a nonpermissive temperature, showing a defect(s) in the respiratory electron transport chain of mitochondria. Of the respiratory chain complexes, rotenone-sensitive NADH-ubiquinone reductase (Complex I) was most severely impaired in the mutant, whereas its activity was restored in a revertant of the mutant that had regained the ability to synthesize CL. These results suggest that CL plays a critical role in mitochondrial functions, at least in the respiratory electron transport chain.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
25
pubmed:volume
268
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
22914-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Mitochondrial dysfunction of a cultured Chinese hamster ovary cell mutant deficient in cardiolipin.
pubmed:affiliation
Department of Biochemistry and Cell Biology, National Institute of Health, Tokyo, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't