Document Detail

Effects of increasing intracellular reactive iron level on cardiac function and oxidative injury in the isolated rat heart.
MedLine Citation:
PMID:  8877786     Owner:  NLM     Status:  MEDLINE    
Elevation of cell iron content was produced by use of a lipophilic iron ligand, 8-hydroxyquinoline (HQ), capable of transferring catalytically active iron into cells. The Fe(3+)-HQ complex labeled with 59Fe was avidly taken up by isolated perfused hearts contrary to the hydrophilic complex Fe(3+)-citrate. Hearts perfused in aerobic conditions with Krebs-Henseleit buffer were exposed for 15 min to the iron complexes, Fe(3+)-HQ (5 microM/10 microM and 10 microM/20 microM), or Fe(3+)-citrate (10 microM), and then perfused for 30 min with normal buffer. Exposure to the high dose of Fe(3+)-HQ (10 microM/20 microM) resulted in early and irreversible decreases in coronary flow and heart rate (-48% and -33%, respectively), initial increases followed by decreases in left ventricular systolic pressure and +dP/dt, and increase in left ventricular end-diastolic pressure (+80%). The low dose of Fe(3+)-HQ (5 microM/10 microM) mimicked with a lower magnitude the effects of the high dose, whereas Fe(3+)-citrate had no effects on cardiac parameters. Only hearts exposed to the high dose of Fe(3+)-HQ exhibited a significant increase (+60%) in thiobarbituric acid-reactive substance level, an index of lipid peroxidation. The production of hydroxyl radicals was investigated by measuring 2,3-dihydroxybenzoic acid level in the coronary effluent after addition of salicylic acid (1 mM) in the perfusate. An immediate and high increase (x6) was seen during heart exposure to Fe(3+)-HQ (10 microM/20 microM) and to Fe(3+)-citrate (10 microM). Considering Fe(3+)-citrate had no effect on cardiac function and lipid peroxidation it was concluded that this hydroxyl radical formation occurring in the extracellular space was not implicated in Fe(3+)-HQ-induced cardiac dysfunction. These results demonstrate the deleterious effect of increasing intracellular reactive iron level in non-ischemic hearts.
M Oubidar; C Marie; C Mossiat; J Bralet
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Publication Detail:
Type:  In Vitro; Journal Article    
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  28     ISSN:  0022-2828     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  1996 Aug 
Date Detail:
Created Date:  1997-01-29     Completed Date:  1997-01-29     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:  1769-76     Citation Subset:  IM    
Laboratoire de Pharmacodynamie, Faculté de Pharmacie, Dijon, France.
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MeSH Terms
Coronary Circulation / drug effects*
Free Radicals
Heart Rate / drug effects*
Hydroxyl Radical
Iron / metabolism*
Lipid Peroxidation / drug effects,  physiology
Myocardium / cytology,  metabolism*
Oxidative Stress / physiology*
Oxyquinoline / pharmacology
Rats, Wistar
Reactive Oxygen Species / metabolism*
Thiobarbituric Acid Reactive Substances / metabolism
Reg. No./Substance:
0/Free Radicals; 0/Reactive Oxygen Species; 0/Thiobarbituric Acid Reactive Substances; 148-24-3/Oxyquinoline; 3352-57-6/Hydroxyl Radical; 7439-89-6/Iron

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