title: Trace elements and cardioprotection: increasing endogenous glutathione peroxidase activity by oral selenium supplementation in rats limits reperfusion-induced arrhythmias.
abstract: Oxyradicals have been implicated as a possible cause of reperfusion-arrhythmias (RA). However, the use of diverse exogenous oxyradical scavengers designed to reduce RA has given contradictory results. The aim of the present study was to determine whether enhancing the activity of the main endogenous enzyme involved in peroxide elimination in cardiac cells, namely glutathione peroxidase, may limit RA in isolated heart preparations by increasing their antioxidant status. For this purpose, a group of 15 male Wistar rats received a selenium enriched diet for ten weeks (1.5 mg Se/kg diet). Control animals (n = 15) received a standard diet containing 0.05 mg Se/kg diet. The incidence of early ventricular arrhythmias was investigated during the reperfusion period following 10 min regional ischemia induced ex-vivo by left coronary artery ligation. Our results show that selenium-supplementation significantly increased the global selenium status of the animals. In the isolated heart preparations, the selenium supplementation induced a significant reduction of the severity of RA as assessed by the arrhythmia score and the limitation of the incidence of both ventricular tachycardia (control: 91% vs selenium: 36%, p < 0.05) and irreversible ventricular fibrillation (control: 45% vs selenium: 0%, p < 0.05). These effects were associated with a significant increase in cardiac mitochondrial and cytosolic glutathione peroxidase activities in both the left and the right ventricles. These results illustrate the potential protective effect of selenium against ischemia-reperfusion injury and suggest that peroxides might play a key role in the genesis of some aspects of the reperfusion syndrome.
authors.affiliation: Physiopathologie Cellulaire Cardiaque, CNRS ESA 5077, Université J. Fourier, Grenoble, France.
authors.forename: S
authors.initials: S
authors.lastname: Tanguy
authors.forename: F
authors.initials: F
authors.lastname: Boucher
authors.forename: S
authors.initials: S
authors.lastname: Besse
authors.forename: V
authors.initials: V
authors.lastname: Ducros
authors.forename: A
authors.initials: A
authors.lastname: Favier
authors.forename: J
authors.initials: J
authors.lastname: de Leiris
mesh_terms: D000284:Administration, Oral; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000517:prevention & control*; D001835:Body Weight / Q000187:drug effects; D002317:Cardiovascular Agents / Q000008:administration & dosage*; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology; D019587:Dietary Supplements; D004912:Erythrocytes / Q000378:metabolism; D005609:Free Radicals; D005979:Glutathione Peroxidase / Q000378:metabolism*; D006321:Heart / Q000033:anatomy & histology / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D009206:Myocardium / Q000201:enzymology* / Q000378:metabolism; D009929:Organ Size / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D012643:Selenium / Q000008:administration & dosage* / Q000097:blood
chemical_list: D002317:Cardiovascular Agents; D005609:Free Radicals; D017382:Reactive Oxygen Species; D005979:Glutathione Peroxidase; D012643:Selenium