Document Detail


Poly(ADP-ribose) polymerase inhibition prevents both apoptotic-like delayed neuronal death and necrosis after H(2)O(2) injury.
MedLine Citation:
PMID:  12091461     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Toxic reactive oxygen species (ROS) such as hydrogen peroxide, nitric oxide, superoxide, and the hydroxyl radical are generated in a variety of neuropathological conditions and cause significant DNA damage. We determined the effects of 3-aminobenzamide (AB), an inhibitor of the DNA repair enzyme poly(ADP-ribose) polymerase (PARP), on cell death in differentiated PC12 cells, a model of sympathetic neurons, after H(2) O(2) injury. Exposure to 0.5 mm H(2) O(2) resulted in a significant decrease in intracellular NAD(H), NADP(H), and ATP levels. This injury resulted in the death of 90% of the cells with significant necrosis early (2 h) after injury and increased apoptosis (12-24 h after injury), as measured by PS exposure and the presence of cytoplasmic oligonucleosomal fragments. Treatment with 2.5 mm AB restored pyridine nucleotide and ATP levels and ameliorated cell death (65% versus 90%) by decreasing the extent of both necrosis and apoptosis. Interestingly, we observed that H(2) O(2) -induced injury caused a delayed cell death exhibiting features of apoptosis but in which caspase-3 like activity was absent. Moreover, pretreatment with AB restored caspase-3-like activity. Our results suggest that apoptosis and necrosis are both triggered by PARP overactivation, and that maintenance of cellular energy levels after injury by inhibiting PARP shifts cell death from necrosis to apoptosis.
Authors:
Kasie K Cole; J Regino Perez-Polo
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of neurochemistry     Volume:  82     ISSN:  0022-3042     ISO Abbreviation:  J. Neurochem.     Publication Date:  2002 Jul 
Date Detail:
Created Date:  2002-07-01     Completed Date:  2002-08-05     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  2985190R     Medline TA:  J Neurochem     Country:  England    
Other Details:
Languages:  eng     Pagination:  19-29     Citation Subset:  IM    
Affiliation:
Department of Anatomy and Neurosciences, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-0652, USA.
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / metabolism
Animals
Apoptosis / drug effects*
Benzamides / pharmacology*
Caspase 3
Caspases / metabolism
Cell Death / drug effects
Cell Survival / drug effects
DNA Fragmentation / drug effects
Dose-Response Relationship, Drug
Enzyme Inhibitors / pharmacology
Hydrogen Peroxide / toxicity*
NAD / metabolism
NADP / metabolism
Necrosis*
Neurons / cytology,  drug effects*,  enzymology
Neuroprotective Agents / pharmacology
PC12 Cells
Poly Adenosine Diphosphate Ribose / biosynthesis
Poly(ADP-ribose) Polymerases / antagonists & inhibitors*,  metabolism
Rats
Grant Support
ID/Acronym/Agency:
P01 NS 39161/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Benzamides; 0/Enzyme Inhibitors; 0/Neuroprotective Agents; 26656-46-2/Poly Adenosine Diphosphate Ribose; 3544-24-9/3-aminobenzamide; 53-59-8/NADP; 53-84-9/NAD; 56-65-5/Adenosine Triphosphate; 7722-84-1/Hydrogen Peroxide; EC 2.4.2.30/Poly(ADP-ribose) Polymerases; EC 3.4.22.-/Casp3 protein, rat; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspases

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


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