Document Detail


Superoxide dismutase (SOD) as a potential inhibitory mediator of inflammation via neutrophil apoptosis.
MedLine Citation:
PMID:  16036355     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Superoxide dismutase (SOD) is supposed to be an effective agent for neutrophil-mediated inflammation in the area of critical medicine. We investigated the involvement of SOD in the regulation of neutrophil apoptosis. Exogenously added SOD effectively induced neutrophil apoptosis, and the fluorescence patterns determined using annexin-V and the 7-AAD were similar to those seen in Fas-mediated neutrophil apoptosis. Neutrophils are short-lived leukocytes that need to be removed safely by apoptosis. The clearance of apoptotic neutrophils from sites of inflammation is a crucial determinant of the resolution of inflammation. Catalase inhibited the neutrophil apoptosis and caspase-3 activation. Spontaneous apoptosis, hydrogen peroxide and anti-Fas antibody-induced apoptosis of neutrophils were accelerated in Down's syndrome patients, in whom the SOD gene is overexpressed. Hydrogen peroxide was thought to be a possible major mediator of ROS-induced neutrophil apoptosis in caspase-dependent manner. Neutrophil apoptosis represents a crucial step in the mechanism governing the resolution of inflammation and has been suggested as a possible target for the control of neutrophil-mediated tissue injury. SOD may be a potential inhibitory mediator of neutrophil-mediated inflammation.
Authors:
Kozo Yasui; Norimoto Kobayashi; Takashi Yamazaki; Kazunaga Agematsu; Satoshi Matsuzaki; Susumu Ito; Setsuko Nakata; Atsushi Baba; Kenichi Koike
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Free radical research     Volume:  39     ISSN:  1071-5762     ISO Abbreviation:  Free Radic. Res.     Publication Date:  2005 Jul 
Date Detail:
Created Date:  2005-07-22     Completed Date:  2005-10-25     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9423872     Medline TA:  Free Radic Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  755-62     Citation Subset:  IM    
Affiliation:
Department of Pediatrics, Shinshu University School of Medicine, Asahi 3-1-1, Matsumoto, 390-8621, Japan. k-yasui@hsp.md.shinshu-u.ac.jp
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MeSH Terms
Descriptor/Qualifier:
Adult
Annexin A5 / analysis
Antibodies, Monoclonal / pharmacology
Apoptosis / drug effects*,  immunology
Caspase 3
Caspases / metabolism
Down Syndrome / blood,  enzymology
Enzyme Activation
Flow Cytometry
Humans
Inflammation / blood
Neutrophils / cytology*,  drug effects*,  enzymology,  immunology
Reactive Oxygen Species / metabolism
Superoxide Dismutase / pharmacology*
Chemical
Reg. No./Substance:
0/Annexin A5; 0/Antibodies, Monoclonal; 0/Reactive Oxygen Species; 0/anti-Fas monoclonal antibody; EC 1.15.1.1/Superoxide Dismutase; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspases

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