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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
1996-9-10
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pubmed:abstractText |
A 3 h exposure to 1 mM H2O2 followed by 6 h post-challenge growth in peroxide-free medium induces necrosis in U937 cells. Addition of the poly(ADP-ribose)polymerase inhibitor 3-aminobenzamide during recovery prevents necrosis and triggers apoptosis, as shown by the appearance of apoptotic bodies, extensive blebbing and formation of multimeric DNA fragments as well as 50 kb double stranded DNA fragments. Thus, the same initial damage can be a triggering event for both apoptotic and necrotic cell death. Furthermore, necrosis does not appear to be a passive response to overwhelming damage.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0014-5793
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
390
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
91-4
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8706837-Apoptosis,
pubmed-meshheading:8706837-Benzamides,
pubmed-meshheading:8706837-Cell Line,
pubmed-meshheading:8706837-Culture Media,
pubmed-meshheading:8706837-DNA, Neoplasm,
pubmed-meshheading:8706837-Enzyme Inhibitors,
pubmed-meshheading:8706837-Humans,
pubmed-meshheading:8706837-Hydrogen Peroxide,
pubmed-meshheading:8706837-Kinetics,
pubmed-meshheading:8706837-Leukemia, Myeloid,
pubmed-meshheading:8706837-Necrosis,
pubmed-meshheading:8706837-Oxidative Stress,
pubmed-meshheading:8706837-Poly(ADP-ribose) Polymerases,
pubmed-meshheading:8706837-Time Factors,
pubmed-meshheading:8706837-Tumor Cells, Cultured
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pubmed:year |
1996
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pubmed:articleTitle |
Prevention of necrosis and activation of apoptosis in oxidatively injured human myeloid leukemia U937 cells.
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pubmed:affiliation |
Istituto di Farmacologia e Farmacognosia and Centro di Farmacologia Oncologica Sperimentale, Università di Urbino, Italy.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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