Document Detail

Aminothiol redox alterations in patients with chronic heart failure of ischaemic or non-ischaemic origin.
MedLine Citation:
PMID:  18163014     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: Oxidative stress plays a role in the progression of chronic heart failure (CHF), but whether and how ischaemic heart disease (IHD) or non-IHD aetiology may account for differential redox alterations is currently unclear. We assessed the relation between thiol redox state and lipid peroxidation, as a marker of oxidative stress, in patients with CHF of ischaemic or non-ischaemic origin. METHODS: Blood reduced glutathione, plasma total and reduced cysteine, cysteinylglycine, homocysteine, glutathione, plasma alpha-tocopherol, ascorbic acid, and free malondialdehyde were assessed in 43 CHF heart transplant candidates (24 IHD and 19 non-IHD) and 30 controls matched for age, gender and number of atherosclerotic risk factors. RESULTS: Reduced cysteine was increased in CHF patients compared with controls. The highest levels were found in IHD versus non-IHD patients versus controls. Malondialdehyde levels were significantly higher in IHD patients than in controls, whereas antioxidant vitamins did not differ among the three groups. CONCLUSIONS: Specific abnormalities in the thiol pattern are associated with heart failure aetiology in CHF patients. Our findings point to the possible role of reduced cysteine in the progression of chronic IHD to heart failure status, as an additional pro-oxidant stimulus for worsening oxidative stress.
Jonica Campolo; Raffaele Caruso; Renata De Maria; Marina Parolini; Fabrizio Oliva; Elena Roubina; Giuliana Cighetti; Maria Frigerio; Ettore Vitali; Oberdan Parodi
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of cardiovascular medicine (Hagerstown, Md.)     Volume:  8     ISSN:  1558-2027     ISO Abbreviation:  J Cardiovasc Med (Hagerstown)     Publication Date:  2007 Dec 
Date Detail:
Created Date:  2007-12-28     Completed Date:  2008-01-24     Revised Date:  2009-05-28    
Medline Journal Info:
Nlm Unique ID:  101259752     Medline TA:  J Cardiovasc Med (Hagerstown)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1024-8     Citation Subset:  IM    
CNR Clinical Physiology Institute of Milan, Cardiology Department, Niguarda Ca Granda Hospital, Milan, Italy.
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MeSH Terms
Ascorbic Acid / blood
Biological Markers / blood
Case-Control Studies
Chronic Disease
Cysteine / blood
Dipeptides / blood
Disease Progression
Glutathione / blood
Heart Failure / blood*,  etiology
Homocysteine / blood
Lipid Peroxidation*
Malondialdehyde / blood
Middle Aged
Myocardial Ischemia / blood,  complications*
Oxidative Stress*
Research Design
Sulfhydryl Compounds / blood*
alpha-Tocopherol / blood
Reg. No./Substance:
0/Biological Markers; 0/Dipeptides; 0/Sulfhydryl Compounds; 19246-18-5/cysteinylglycine; 454-28-4/Homocysteine; 50-81-7/Ascorbic Acid; 52-90-4/Cysteine; 542-78-9/Malondialdehyde; 59-02-9/alpha-Tocopherol; 70-18-8/Glutathione

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

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