title: Effect of dietary selenium on the progression of heart failure in the ageing spontaneously hypertensive rat.
abstract: Oxidative stress has been directly implicated in hypertension and myocardial remodelling, two pathologies fundamental to the development of chronic heart failure. Selenium (Se) can act directly and indirectly as an antioxidant and a lowered Se status leads to a higher risk of cardiovascular disease. This study examined the role of Se on the development of hypertension and subsequent progression to chronic heart failure in spontaneously hypertensive rats (SHR). Three dietary groups were studied: (i) Se-free; (ii) normal Se (50 μg Se/kg food); and (iii) high Se (1000 μg Se/kg food). Systolic blood pressure and echocardiography were used to detect cardiac changes in vivo. At study end, cardiac tissues were assayed for glutathione peroxidase activity, thioredoxin reductase activity, and protein carbonyls. The major finding of this study was the high heart failure-related mortality rate in SHRs fed an Se-free diet (70%). Normal and high levels of dietary Se resulted in higher survival rates of 78 and 100%, respectively. Furthermore, high dietary Se was clearly associated with lower levels of cardiac oxidative damage and increased antioxidant expression, as well as a reduction in disease severity and mortality in the SHR.
authors.affiliation: Heart Foundation Research Centre, School of Medical Science, Griffith University, Southport, Queensland, Australia.
authors.forename: Robyn S
authors.initials: RS
authors.lastname: Lymbury
authors.forename: Matthew J
authors.initials: MJ
authors.lastname: Marino
authors.forename: Anthony V
authors.initials: AV
authors.lastname: Perkins
mesh_terms: D000375:Aging; D000818:Animals; D001794:Blood Pressure; D003677:Deficiency Diseases / Q000150:complications / Q000401:mortality; D004032:Diet / Q000009:adverse effects; D018450:Disease Progression; D005979:Glutathione Peroxidase / Q000378:metabolism; D006333:Heart Failure / Q000150:complications / Q000178:diet therapy* / Q000401:mortality / Q000503:physiopathology; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000473:pathology; D006973:Hypertension / Q000150:complications / Q000401:mortality / Q000503:physiopathology*; D008297:Male; D009206:Myocardium / Q000201:enzymology; D018384:Oxidative Stress; D050050:Protein Carbonylation; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D012643:Selenium / Q000008:administration & dosage* / Q000172:deficiency; D016019:Survival Analysis; D013880:Thioredoxin-Disulfide Reductase / Q000378:metabolism; D014463:Ultrasonography
chemical_list: D005979:Glutathione Peroxidase; D013880:Thioredoxin-Disulfide Reductase; D012643:Selenium