Document Detail


Mitochondrial involvement in nitric oxide-induced cellular death in cortical neurons in culture.
MedLine Citation:
PMID:  16397899     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Nitric oxide (NO) is an unstable molecule with physiological and pathological properties. In brain, NO acts as a modulator of neurotransmission as well as a protector against neuronal death from several death stimuli. However, beside this protector effect, high NO concentrations produce neuronal death by a mechanism in which the caspase pathway is implicated. In this work, we demonstrate that in cortical neurons the NO toxicity is mediated by mitochondrial dysfunction. SNAP, an NO donor, induces apoptosis in these cells because it 1) increases the p53 and 2) induces cytochrome c release and activation of caspase-9 and caspase-3. SNAP also induces necrosis, through 1) breakdown of the mitochondrial membrane potential, 2) ATP decrease, 3) ROS formation, and 4) LDH and ATP release, indicative of oxidative stress and death by necrosis. To sum up, in cortical neurons, high NO concentrations produced cellular death by both an apoptotic and a necrotic mechanism in which the mitochondria are implicated.
Authors:
S Figueroa; M J Oset-Gasque; C Arce; C J Martinez-Honduvilla; M P González
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of neuroscience research     Volume:  83     ISSN:  0360-4012     ISO Abbreviation:  J. Neurosci. Res.     Publication Date:  2006 Feb 
Date Detail:
Created Date:  2006-02-02     Completed Date:  2006-05-25     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  7600111     Medline TA:  J Neurosci Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  441-9     Citation Subset:  IM    
Affiliation:
Instituto de Bioquímica (Centro Mixto CSIC-UCM), Facultad de Farmacia, Ciudad Universitaria, Madrid, Spain.
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / metabolism
Animals
Benzoates / pharmacology
Blotting, Western / methods
Caspase 3
Caspase 9
Caspases / metabolism
Cell Death / drug effects
Cell Survival / drug effects
Cells, Cultured
Cerebral Cortex / cytology*
Cytochromes / metabolism
Dose-Response Relationship, Drug
Drug Interactions
Embryo, Mammalian
Imidazoles / pharmacology
Intracellular Space / drug effects*
L-Lactate Dehydrogenase / metabolism
Membrane Potentials / drug effects
Mitochondria / physiology*
Neuroglia / drug effects
Neurons / drug effects*
Nitric Oxide / pharmacology*
Nitric Oxide Donors / pharmacology
Penicillamine / analogs & derivatives,  pharmacology
Rats
Reactive Oxygen Species / metabolism
Tumor Suppressor Protein p53 / metabolism
Ubiquitin-Protein Ligase Complexes / pharmacology
Chemical
Reg. No./Substance:
0/Benzoates; 0/Cytochromes; 0/Imidazoles; 0/Nitric Oxide Donors; 0/Reactive Oxygen Species; 0/S-nitro-N-acetylpenicillamine; 0/Tumor Suppressor Protein p53; 10102-43-9/Nitric Oxide; 145757-47-7/1,3-dihydroxy-4,4,5,5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole; 52-67-5/Penicillamine; 56-65-5/Adenosine Triphosphate; EC 1.1.1.27/L-Lactate Dehydrogenase; EC 3.4.22.-/Casp3 protein, rat; EC 3.4.22.-/Casp9 protein, rat; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspase 9; EC 3.4.22.-/Caspases; EC 6.3.2.19/Ubiquitin-Protein Ligase Complexes; EC 6.3.2.19/anaphase-promoting complex

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


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