title: Aminothiol redox alterations in patients with chronic heart failure of ischaemic or non-ischaemic origin.
abstract: 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.
authors.affiliation: CNR Clinical Physiology Institute of Milan, Cardiology Department, Niguarda Ca Granda Hospital, Milan, Italy.
authors.forename: Jonica
authors.initials: J
authors.lastname: Campolo
authors.forename: Raffaele
authors.initials: R
authors.lastname: Caruso
authors.forename: Renata
authors.initials: R
authors.lastname: De Maria
authors.forename: Marina
authors.initials: M
authors.lastname: Parolini
authors.forename: Fabrizio
authors.initials: F
authors.lastname: Oliva
authors.forename: Elena
authors.initials: E
authors.lastname: Roubina
authors.forename: Giuliana
authors.initials: G
authors.lastname: Cighetti
authors.forename: Maria
authors.initials: M
authors.lastname: Frigerio
authors.forename: Ettore
authors.initials: E
authors.lastname: Vitali
authors.forename: Oberdan
authors.initials: O
authors.lastname: Parodi
mesh_terms: D000368:Aged; D001205:Ascorbic Acid / Q000097:blood; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D002908:Chronic Disease; D003545:Cysteine / Q000097:blood; D004151:Dipeptides / Q000097:blood; D018450:Disease Progression; D005260:Female; D005978:Glutathione / Q000097:blood; D006333:Heart Failure / Q000097:blood* / Q000209:etiology; D006710:Homocysteine / Q000097:blood; D006801:Humans; D015227:Lipid Peroxidation; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000097:blood / Q000150:complications*; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D012107:Research Design; D013438:Sulfhydryl Compounds / Q000097:blood*; D024502:alpha-Tocopherol / Q000097:blood
chemical_list: D015415:Biomarkers; D004151:Dipeptides; D013438:Sulfhydryl Compounds; D006710:Homocysteine; C028505:cysteinylglycine; D008315:Malondialdehyde; D005978:Glutathione; D024502:alpha-Tocopherol; D003545:Cysteine; D001205:Ascorbic Acid