title: Dietary selenium intake influences Cx43 dephosphorylation, TNF-α expression and cardiac remodeling after reperfused infarction.
abstract: METHODS
  Post-infarct left ventricular dysfunction and cardiac remodeling are the primary causes of chronic heart failure in industrialized countries. In the present study, we examined the influence of dietary selenium intake on cardiac remodeling after reperfused myocardial infarction and explored one of the possible mechanisms.
  
  
  RESULTS
  Rats were fed a diet containing either 0.05 mg/kg (Low-Se, group of rats receiving the low-selenium diet) or 1.50 mg/kg (group of rats receiving the high-selenium diet) selenium. At the end of the 5th week of the diet, rats were subjected to transient (1 h) coronary ligation followed by 8 days of reperfusion. Infarct size and cardiac passive compliance were increased in the Low-Se group compared with group of rats receiving the high-selenium diet. Similarly, indices of cardiac remodeling (thinning index and expansion index) were more altered in Low-Se hearts. These adverse effects of the Low-Se diet on cardiac remodeling were accompanied by an increase in cardiac TNF-α content, a decreased activity of antioxidant seleno-enzymes and an increase in connexin-43 dephosphorylation.
  
  
  CONCLUSIONS
  Dietary selenium intake influences post-infarct cardiac remodeling even when provided within the range of physiological values. Our data suggest that the cardioprotective effect of selenium might be mediated by a reduced oxidative stress, a lower connexin-43 dephosphorylation, and a decreased TNF-α expression.
authors.affiliation: Laboratoire TIMC-IMAG, UMR 5525 CNRS - University of Grenoble, Grenoble, France.
authors.forename: Stéphane
authors.initials: S
authors.lastname: Tanguy
authors.forename: Andry
authors.initials: A
authors.lastname: Rakotovao
authors.forename: Marie-Gabrielle
authors.initials: MG
authors.lastname: Jouan
authors.forename: Catherine
authors.initials: C
authors.lastname: Ghezzi
authors.forename: Joël
authors.initials: J
authors.lastname: de Leiris
authors.forename: François
authors.initials: F
authors.lastname: Boucher
mesh_terms: D000818:Animals; D003187:Compliance; D018031:Connexin 43 / Q000378:metabolism*; D003677:Deficiency Diseases / Q000503:physiopathology; D004032:Diet; D005979:Glutathione Peroxidase / Q000378:metabolism; D006352:Heart Ventricles / Q000737:chemistry / Q000503:physiopathology; D008297:Male; D009124:Muscle Proteins / Q000378:metabolism; D015428:Myocardial Reperfusion Injury / Q000097:blood / Q000378:metabolism* / Q000503:physiopathology / Q000517:prevention & control; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D010766:Phosphorylation; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D012643:Selenium / Q000008:administration & dosage* / Q000097:blood / Q000172:deficiency / Q000627:therapeutic use; D013880:Thioredoxin-Disulfide Reductase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*; D018487:Ventricular Dysfunction, Left / Q000517:prevention & control; D020257:Ventricular Remodeling
chemical_list: D018031:Connexin 43; D009124:Muscle Proteins; D014409:Tumor Necrosis Factor-alpha; D005979:Glutathione Peroxidase; D013880:Thioredoxin-Disulfide Reductase; D012643:Selenium