Document Detail


Antimycin A-induced cell death depends on AIF translocation through NO production and PARP activation and is not involved in ROS generation, cytochrome c release and caspase-3 activation in HL-60 cells.
MedLine Citation:
PMID:  19229286     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A respiratory inhibitor, antimycin A (AA), induced an apoptotic-like cell death characterized by nuclear and DNA fragmentation in human leukemia HL-60 cells. This cell death was significantly restricted by a nitric oxide synthase (NOS) inhibitor, N(G)-monomethyl-L-arginine (L-NMMA), and a poly(ADP-ribose) polymerase (PARP) inhibitor, 5-aminoisoquinoline (AIQ). Indeed, NO production and PARP overactivation were detected in the cells treated with AA. On the one hand, L-NMMA partly eliminated NO production and on the other, AIQ and L-NMMA also restricted PARP activation. Excessive signals related to PARP overactivation induce the translocation of an apoptosis-inducing factor (AIF) from the mitochondria to the nuclei, resulting in DNA fragmentation. In AA-treated cells, the nuclear translocation of AIF occurred. This translocation was restricted by pretreatment with AIQ and L-NMMA. Although pretreatment with ascorbic acid eliminated the reactive oxygen species (ROS) generation induced by the blockade of complex III by AA, the pretreatment did not protect the cells from AA-induced cell death. Furthermore, cytochrome c release or caspase-3 activation was not observed in the cells treated with AA. These results suggest that AA-induced cell death does not depend on respiratory inhibition and the succeeding cascades, but on NO production, PARP overactivation and AIF translocation.
Authors:
Masaki Ogita; Akira Ogita; Yoshinosuke Usuki; Ken-ichi Fujita; Toshio Tanaka
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Publication Detail:
Type:  Journal Article     Date:  2009-02-20
Journal Detail:
Title:  The Journal of antibiotics     Volume:  62     ISSN:  0021-8820     ISO Abbreviation:  J. Antibiot.     Publication Date:  2009 Mar 
Date Detail:
Created Date:  2009-03-27     Completed Date:  2009-10-19     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0151115     Medline TA:  J Antibiot (Tokyo)     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  145-52     Citation Subset:  IM    
Affiliation:
Department of Biology and Geosciences, Graduate School of Science, Osaka City University, Sumiyoshi-ku, Osaka, Japan.
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MeSH Terms
Descriptor/Qualifier:
Antibiotics, Antineoplastic / pharmacology*
Antimycin A / pharmacology*
Apoptosis Inducing Factor / metabolism*
Calpain / metabolism
Caspase 3 / metabolism*
Cell Death / drug effects
Cell Nucleus / drug effects,  ultrastructure
Cytochromes c / metabolism*
Cytosol / drug effects,  metabolism
DNA Fragmentation / drug effects
Enzyme Activation / drug effects
Fluorescent Dyes
HL-60 Cells
Humans
Membrane Potentials / drug effects
NAD / metabolism
Nitric Oxide / biosynthesis*
Poly(ADP-ribose) Polymerases / metabolism*
Protein Transport
Reactive Oxygen Species / metabolism*
Chemical
Reg. No./Substance:
0/Antibiotics, Antineoplastic; 0/Apoptosis Inducing Factor; 0/Fluorescent Dyes; 0/Reactive Oxygen Species; 10102-43-9/Nitric Oxide; 53-84-9/NAD; 642-15-9/Antimycin A; 9007-43-6/Cytochromes c; EC 2.4.2.30/Poly(ADP-ribose) Polymerases; EC 3.4.22.-/Calpain; EC 3.4.22.-/Caspase 3

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


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