Document Detail

Mediatory role of copper in reactive oxygen intermediate-induced cardiac injury.
MedLine Citation:
PMID:  1479626     Owner:  NLM     Status:  MEDLINE    
In this report the mediatory role of copper in cardiac injury produced by reactive oxygen intermediates was examined. Isolated rat hearts were perfused with Krebs-Henseleit buffer containing 0.25 mM ascorbate plus varying concentrations of copper-bis-histidial for up to 60 min. Using salicylate as a probe, OH generation by this system was demonstrated. Copper or ascorbate alone had minimal effect on cardiac function as determined by heart rate, coronary flow, left ventricular systolic pressure development, end diastolic pressure and +/- dP/dtmax. Copper, from 0.5 microM to 20 microM, and ascorbate, 0.25 mM, resulted in concentration-dependent decreases in all of the experimental variables. Treatment with 5 or 20 microM copper resulted in complete loss of cardiac function within 40 and 30 min, respectively. By 30 min, 5 microM copper had resulted in increased end diastolic pressure to greater than 40 mmHg. By 60 min, perfusion with 1 microM copper resulted in almost 100% loss of function and end diastolic pressure greater than 25 mmHg. Copper, 0.5 microM, also decreased cardiac function, but to a lesser degree. Catalase, 100 units/ml, was effective in preventing the copper-ascorbate induced cardiac damage while superoxide dismutase, 25 units/ml, was ineffective. Observations by light and electron microscopy demonstrated patchy regions with vacuolization corresponding to swollen mitochondria. These results clearly demonstrate that copper-catalyzed redox reactions can induce cardiac injury via a mechanism which appears to be related to the production of OH.
S R Powell; L Hyacinthe; S Teichberg; A J Tortolani
Related Documents :
2925356 - Protective effect of branched chain-enriched amino acid formulation in myocardial ische...
8490936 - Ultrastructural demonstration of peroxidative activity and peroxidation in ischaemic an...
22533546 - Three-year safety and effectiveness of fixed-dose losartan/hydrochlorothiazide combinat...
22422296 - Effusive-constrictive pericarditis.
1625376 - Systems analysis of the carotid sinus baroreflex system using a sum-of-sinusoidal input.
23126346 - Impact of the number of blood pressure measurements on blood pressure classification in...
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  24     ISSN:  0022-2828     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  1992 Nov 
Date Detail:
Created Date:  1993-02-11     Completed Date:  1993-02-11     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  1371-86     Citation Subset:  IM    
Department of Surgery, North Shore University Hospital, Manhasset, NY 11030.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Ascorbic Acid / pharmacology
Copper / metabolism*,  pharmacology
Free Radical Scavengers
Heart / drug effects,  physiopathology
Microscopy, Electron
Myocardial Reperfusion Injury / etiology*,  metabolism,  pathology
Rats, Sprague-Dawley
Reactive Oxygen Species / metabolism*
Reg. No./Substance:
0/Free Radical Scavengers; 0/Reactive Oxygen Species; 50-81-7/Ascorbic Acid; 7440-50-8/Copper

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

Previous Document:  Pyrimidine nucleotide synthesis is preferentially supplied by exogenous cytidine in adult rat cultur...
Next Document:  Cocaine and speedball users: differences in psychopathology.