Document Detail

Nucleotide requirement and effects of fatty acids on protein synthesis and degradation in brown adipose tissue mitochondria.
MedLine Citation:
PMID:  8513430     Owner:  NLM     Status:  MEDLINE    
The objective of this work was to evaluate whether changes in respiratory status of isolated brown-fat mitochondria influence synthesis and degradation of proteins within the organelles. Mitochondrial protein synthesis is subject to regulation, as a 24-h fast in mice reduced [35S]methionine incorporation without affecting the stability of the newly synthesized proteins. Proteins synthesized in isolated mitochondria were labile and degraded in a process stimulated by ATP. ATP hydrolysis was required within the organelle, as ATP-stimulated protein breakdown was inhibited by atractyloside, an inhibitor of adenine nucleotide transport, and by arsenate and vanadate, which inhibit ATPases. Additions of ATP and ADP were equally effective at reducing mitochondrial oxygen consumption. However, ATP added exogenously was better at supporting protein synthesis and degradation than ATP generated by oxidative phosphorylation when mitochondria were incubated with ADP, substrates, and Pi. GDP also reduced oxygen consumption and stimulated degradation of mitochondrial translation products. Addition of fatty acids in the presence or absence of carnitine-CoA increased mitochondrial respiration but had no effect on protein synthesis or degradation. Addition of carbonyl cyanide m-chlorophenylhydrazone (mCCP) had no effect on ATP-stimulated protein degradation. These results indicate that synthesis and stability of mitochondrial translation products are not significantly influenced by changes in the activity of the uncoupling protein brought about by additions of adenine nucleotides and fatty acids.
M Desautels; R A Dulos
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Canadian journal of physiology and pharmacology     Volume:  71     ISSN:  0008-4212     ISO Abbreviation:  Can. J. Physiol. Pharmacol.     Publication Date:  1993 Jan 
Date Detail:
Created Date:  1993-07-21     Completed Date:  1993-07-21     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0372712     Medline TA:  Can J Physiol Pharmacol     Country:  CANADA    
Other Details:
Languages:  eng     Pagination:  17-25     Citation Subset:  IM    
Department of Physiology, College of Medicine, University of Saskatchewan, Saskatoon, Canada.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Adenosine Triphosphate / metabolism
Adipose Tissue, Brown / drug effects,  metabolism*
Antimetabolites / pharmacology
Body Temperature Regulation / drug effects,  physiology
Energy Metabolism / drug effects
Fasting / physiology
Fatty Acids / pharmacology*
Methionine / metabolism
Mitochondria / drug effects,  metabolism*
Nucleotides / metabolism*
Oxygen Consumption / physiology
Protein Biosynthesis
Proteins / metabolism*
Reg. No./Substance:
0/Antimetabolites; 0/Fatty Acids; 0/Nucleotides; 0/Proteins; 56-65-5/Adenosine Triphosphate; 63-68-3/Methionine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Maximal short-term exercise performance and ion regulation in cystic fibrosis.
Next Document:  Intracellular calcium disruption as a secondary event in acetaminophen-induced hepatotoxicity.