Document Detail

Cu,Zn-superoxide dismutase-dependent apoptosis induced by nitric oxide in neuronal cells.
MedLine Citation:
PMID:  10671549     Owner:  NLM     Status:  MEDLINE    
Nitric oxide (NO) challenge to human neuroblastoma cells (SH-SY5Y) ultimately results in apoptosis. Tumor suppressor protein p53 and cell cycle inhibitor p21 accumulate as an early sign of S-nitrosoglutathione-mediated toxicity. Cytochrome c release from mitochondria and caspase 3 activation also occurred. Cells transfected with either wild type (WT) or mutant (G93A) Cu, Zn-superoxide dismutase (Cu,Zn-SOD) produced comparable amounts of nitrite/nitrate but showed different degree of apoptosis. G93A cells were the most affected and WT cells the most protected; however, Cu, Zn-SOD content of these two cell lines was 2-fold the SH-SY5Y cells under both resting and treated conditions. We linked decreased susceptibility of the WT cells to higher and more stable Bcl-2 and decreased reactive oxygen species. Conversely, we linked G93A susceptibility to increased reactive oxygen species production since simultaneous administration of S-nitrosoglutathione and copper chelators protects from apoptosis. Furthermore, G93A cells showed a significant decrease of Bcl-2 expression and, as target of NO-derived radicals, showed lower cytochrome c oxidase activity. These results demonstrate that resistance to NO-mediated apoptosis is strictly related to the level and integrity of Cu,Zn-SOD and that the balance between reactive nitrogen and reactive oxygen species regulates neuroblastoma apoptosis.
M R Ciriolo; A De Martino; E Lafavia; L Rossi; M T Carrì; G Rotilio
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  275     ISSN:  0021-9258     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2000 Feb 
Date Detail:
Created Date:  2000-03-21     Completed Date:  2000-03-21     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  5065-72     Citation Subset:  IM    
Department of Biomedical Sciences, University of Chieti "G. D'Annunzio," via dei Vestini, 66100 Chieti, Italy.
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MeSH Terms
Amyotrophic Lateral Sclerosis / pathology
Apoptosis / physiology*
Caspases / metabolism
Cytochrome c Group / metabolism
Enzyme Activation
Glutathione / analogs & derivatives,  metabolism
Neurons / enzymology,  metabolism*
Nitric Oxide / physiology*
Nitroso Compounds / metabolism
Oncogene Protein p21(ras) / metabolism
Oxidative Stress
Proto-Oncogene Proteins c-bcl-2 / metabolism
Superoxide Dismutase / physiology*
Tumor Cells, Cultured
Tumor Suppressor Protein p53 / metabolism
Reg. No./Substance:
0/Cytochrome c Group; 0/Nitroso Compounds; 0/Proto-Oncogene Proteins c-bcl-2; 0/Tumor Suppressor Protein p53; 10102-43-9/Nitric Oxide; 57564-91-7/S-Nitrosoglutathione; 70-18-8/Glutathione; EC Dismutase; EC 3.4.22.-/Caspases; EC Protein p21(ras)

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

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