Document Detail


Correlation between NO-induced ATP depletion and cytotoxicity in PC12 cells.
MedLine Citation:
PMID:  9779410     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
To ascertain whether NO-elicited cell death is mediated by decreased intracellular ATP, the effect of sodium nitroprusside (SNP), a NO-generator, on ATP content in PC12 cells was examined. After treatment with SNP, the ATP content in PC12 cells was found to decline in a time- and concentration-dependent manner. The decline of ATP content in PC12 cells caused by SNP was found to occur before the appearance of cytotoxicity estimated by MTT staining. In addition, the ATP content of neuronally differentiated PC12 cells, which has been shown to have a higher resistance to SNP than the undifferentiated cells (Nakamura et al., 1997), was less affected by SNP treatment than the undifferentiated cells. These findings suggest that reduction of intracellular ATP content may be one of the mechanisms responsible for the NO toxicity in PC12 cells.
Authors:
M Yasuda; T Uramatsu; H Fujimori; H Pan-Hou
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  The Journal of toxicological sciences     Volume:  23     ISSN:  0388-1350     ISO Abbreviation:  J Toxicol Sci     Publication Date:  1998 Aug 
Date Detail:
Created Date:  1999-01-29     Completed Date:  1999-01-29     Revised Date:  2003-11-14    
Medline Journal Info:
Nlm Unique ID:  7805798     Medline TA:  J Toxicol Sci     Country:  JAPAN    
Other Details:
Languages:  eng     Pagination:  183-8     Citation Subset:  IM    
Affiliation:
Faculty of Pharmaceutical Sciences, Setsunan University, Osaka, Japan.
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / metabolism*
Animals
Cell Death / drug effects*
Cell Differentiation
Dose-Response Relationship, Drug
Drug Resistance, Neoplasm
Nitric Oxide / toxicity*
Nitroprusside / toxicity*
PC12 Cells
Rats
Chemical
Reg. No./Substance:
10102-43-9/Nitric Oxide; 15078-28-1/Nitroprusside; 56-65-5/Adenosine Triphosphate

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


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