Linked Life Data

165276

Source:http://linkedlifedata.com/resource/pubmed/id/165276

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1975-7-31
pubmed:abstractText
Liver cytoplasm from either vitamin E-deficient or normal rats has been shown to suppress mitochondrial respiratory decline induced by microsomes in vitro. The present study is an attempt to identify cytoplasmic factor(s) responsible for this suppression. The effect of cytoplasm from both groups of animals could be removed by trichloroacetate precipitation, boiling, and dialysis against 0.3 M mannitol-o.1 mM Tris buffer, pH 7.4, but not by aging or extraction with isooctane. The addition of oxalacetate of alpha-ketoglutarate plus asparate to cytolplasm potentiated the suppressant effect. Dialyzed cytoplasm was not effective in depressing the respiratory decline. However, the addition of NAD, osalacetate, or alpha-ketoglutarate plus aspartate to dialyzed cytoplasm restored its ability to depress the respiratory decline. When oxalacetate or alpha-ketoglutarate plus aspartate was added to fresh cytoplasm, followed by dialysis, the effect of these compounds was not seen. These results suggest that cytoplasmic factor(s) required for suppression of the respiratory decline were enzymes of the malate shuttle and transamination, which are heat labile and trichloroacetate precipitable, plus the dialyzable metabolites that are associated with these enzymes in the generation of NAD in mitochondria.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0022-3166
pubmed:author
pubmed:issnType
Print
pubmed:volume
105
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
588-94
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1975
pubmed:articleTitle
Vitamin E deficiency in the rat. Cytoplasmic factors required for suppression of mitochondrial respiratory decline.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.