title: Myocardial antioxidant status in chronic alcoholism.
abstract: BACKGROUND
  Excessive ethanol intake is one of the most frequent causes of acquired dilated cardiomyopathy in developed countries. The pathogenesis is multifactorial, with the antioxidant imbalance of cardiac muscle being a potential factor. The current study evaluates myocardial antioxidant status in ethanol consumers and its relation to cardiac damage.
  
  
  METHODS
  The authors assessed superoxide dismutase, glutathione peroxidase, and glutathione reductase enzyme activities as well as the total antioxidant status capacity in myocardial samples obtained from organ donors with sudden death of traumatic or neurological origin. They studied 23 high-dose chronic alcohol consumers, 27 individuals with long-standing hypertension, and 11 healthy controls. Cardiomyopathy was defined according to standard functional and histological criteria.
  
  
  RESULTS
  Patients with dilated cardiomyopathy, either of alcoholic or hypertensive origin, showed increased myocardial superoxide dismutase activities compared with patients without cardiomyopathy (p < 0.001, both) and controls (p < 0.05, both). Total antioxidant status capacity and the activity of glutathione peroxidase and glutathione reductase enzymes were similar in all groups. Superoxide dismutase activity was related to the presence of cardiac enlargement and the degree of cardiac histological damage. The amount and type of alcoholic beverages as well as the nutritional status of the patients were not related to myocardial antioxidant activity.
  
  
  CONCLUSIONS
  The presence of dilated cardiomyopathy, of either alcoholic or hypertensive origin, is related to an increase in myocardial superoxide dismutase activity.
authors.affiliation: Department of Internal Medicine, Hospital Clínic, Institut d'Investigacions Biomèdiques August Pi i Sunyer, University of Barcelona, Barcelona, Spain.
authors.forename: Francesc
authors.initials: F
authors.lastname: Fatjó
authors.forename: Joaquim
authors.initials: J
authors.lastname: Fernández-Solà
authors.forename: Meritxell
authors.initials: M
authors.lastname: Lluís
authors.forename: Montserrat
authors.initials: M
authors.lastname: Elena
authors.forename: Eva
authors.initials: E
authors.lastname: Badía
authors.forename: Emilio
authors.initials: E
authors.lastname: Sacanella
authors.forename: Ramón
authors.initials: R
authors.lastname: Estruch
authors.forename: Josep-María
authors.initials: JM
authors.lastname: Nicolás
mesh_terms: D000437:Alcoholism / Q000201:enzymology / Q000453:epidemiology / Q000378:metabolism*; D000975:Antioxidants / Q000378:metabolism*; D002310:Cardiomyopathy, Alcoholic / Q000201:enzymology / Q000378:metabolism; D002423:Cause of Death; D004452:Echocardiography; D005260:Female; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology; D009752:Nutritional Status; D010084:Oxidation-Reduction; D012907:Smoking; D013318:Stroke Volume; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase