Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1991-7-24
pubmed:abstractText
Liver mitochondria from ethanol-fed rats display an impaired ability for protein synthesis in vitro. Studies were conducted to explore the possible mechanisms which might account for this impaired capacity of ethanol mitochondria for protein synthesis. The present studies did not demonstrate any significant ethanol-induced lesion in mitochondrial nucleic acid metabolism in organelles isolated from ethanol-fed rats for any of the parameters investigated (mtDNA content, steady-state mtRNA concentration, mtRNA polymerase activity, concentration of specific mRNAs and rRNAs, mtRNA processing). An investigation of ribosome function in isolated mitochondria demonstrated significant decreases in the number of active ribosomes (55% fewer) in mitochondria from ethanol-fed rats. Initiation of protein synthesis was also significantly depressed (46%) in ethanol mitochondria. In addition, the yield of ribosomal particles from ethanol mitochondria was decreased 32% as compared to the yield of ribosomal particles from control mitochondria. However, isolated ribosomes from ethanol mitochondria were determined to be fully functional in a poly(U)-directed phenylalanine polymerization system. Soluble translation factors from ethanol mitochondria were also found to support full activity of control ribosomes in a poly(U)-directed phenylalanine polymerization system. These results suggest strongly that the ethanol-induced depression of mitochondrial protein synthesis is due to a decrease in the number of competent ribosomes in hepatic mitochondria from chronically ethanol-fed rats.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0006-3002
pubmed:author
pubmed:issnType
Print
pubmed:day
17
pubmed:volume
1058
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
178-86
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:1710928-Animals, pubmed-meshheading:1710928-Base Sequence, pubmed-meshheading:1710928-Blotting, Northern, pubmed-meshheading:1710928-DNA-Directed RNA Polymerases, pubmed-meshheading:1710928-Electrophoresis, Polyacrylamide Gel, pubmed-meshheading:1710928-Ethanol, pubmed-meshheading:1710928-Liver Diseases, Alcoholic, pubmed-meshheading:1710928-Male, pubmed-meshheading:1710928-Mitochondria, Liver, pubmed-meshheading:1710928-Molecular Sequence Data, pubmed-meshheading:1710928-Oligonucleotide Probes, pubmed-meshheading:1710928-Protein Biosynthesis, pubmed-meshheading:1710928-Protein Synthesis Inhibitors, pubmed-meshheading:1710928-RNA, pubmed-meshheading:1710928-Rats, pubmed-meshheading:1710928-Rats, Inbred Strains, pubmed-meshheading:1710928-Ribosomes, pubmed-meshheading:1710928-Transcription, Genetic
pubmed:year
1991
pubmed:articleTitle
Effect of chronic ethanol consumption on hepatic mitochondrial transcription and translation.
pubmed:affiliation
Department of Biochemistry, Wake Forest University Medical Center, Winston-Salem, NC.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.