Document Detail


The permeability transition pore as a pathway for the release of mitochondrial DNA.
MedLine Citation:
PMID:  15808887     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
This study shows that under oxidative stress DNA from liver mitochondria (mtDNA) can be released through the non-specific permeability transition pore. Pore opening was induced after the addition of Fe2+ and hydrogen peroxide, in the presence of calcium ions. Under these conditions mitochondria undergo large extent swelling, accompanied by the generation of thiobarbituric acid-reactive substances. It was observed that mtDNA was hydrolyzed after the oxidative stress, and it is proposed that some of the fragments were released from the matrix, in such a way that approximately 12% of the total mtDNA remained in the mitochondria. The remaining genetic material was analyzed, after its extraction in an agarose gel. The fragments released were smaller that 1000 bp, by analysis in a native 8% polyacrilamide gel. The presence of cyclosporin A, that inhibited permeability transition, also inhibited mtDNA release by roughly 52%.
Authors:
Noemí García; José J García; Francisco Correa; Edmundo Chávez
Related Documents :
2528667 - The role of calcium in the control of respiration by muscle mitochondria.
4084857 - Cell sonicates used in the analysis of how measles and herpes simplex type 1 virus infe...
1688557 - Stimulation of glycine catabolism in isolated perfused rat liver by calcium mobilizing ...
3452457 - The mechanism and biological role of calcium transport by plant mitochondria.
12199407 - A comparison of the speech understanding provided by acoustic models of fixed-channel a...
12714567 - Blood-brain barrier damage induces release of alpha2-macroglobulin.
Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Life sciences     Volume:  76     ISSN:  0024-3205     ISO Abbreviation:  Life Sci.     Publication Date:  2005 Apr 
Date Detail:
Created Date:  2005-04-05     Completed Date:  2005-05-18     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0375521     Medline TA:  Life Sci     Country:  England    
Other Details:
Languages:  eng     Pagination:  2873-80     Citation Subset:  IM    
Affiliation:
Departamento de Bioquímica, Instituto Nacional de Cardiología, Ignacio Chávez, Juan Badiano #1, México DF 014080, Mexico. ngarciar@salud.gob.mx
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Adenylate Kinase / metabolism
Animals
Biological Transport / drug effects,  physiology
Cyclosporine / pharmacology
DNA, Mitochondrial / metabolism*
Electrophoresis, Agar Gel
Hydrogen Peroxide / toxicity
Iron / toxicity
Lipid Peroxidation / drug effects
Mitochondria, Liver / metabolism*
Mitochondrial Swelling / drug effects*
Oxidative Stress / drug effects*,  physiology
Permeability
Rats
Spectrophotometry
Thiobarbituric Acid Reactive Substances / metabolism
Chemical
Reg. No./Substance:
0/DNA, Mitochondrial; 0/Thiobarbituric Acid Reactive Substances; 59865-13-3/Cyclosporine; 7439-89-6/Iron; 7722-84-1/Hydrogen Peroxide; EC 2.7.4.3/Adenylate Kinase

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


Previous Document:  Downregulation of Rac1 activation by caffeic acid in aortic smooth muscle cells.
Next Document:  Palatability-dependent appetite and benzodiazepines: new directions from the pharmacology of GABA(A)...