Decreasing effects of iron toxicosis on selenium and glutathione peroxidase activity.
Heart failure due to chronic iron overload is a leading cause of cardiovascular mortality in the second and third decades of life worldwide, but its mechanism is not known. Deficiencies of selenium have been shown to result in damage to the myocardium and to the development of various cardiomyopathies. In the current investigation, the dose-dependent effects of chronic iron toxicosis on heart tissue concentrations of selenium and the protective antioxidant enzyme glutathione peroxidase (GPx) were investigated in a murine model of iron-overload cardiomyopathy (n = 20). Significant dose-dependent decreases in heart tissue selenium concentrations (r = -0.95, p < 0.001) and selenium-dependent GPx activity (r = -0.93, p < 0.001) were observed in chronically iron-loaded mice in comparison with placebo controls. These results suggest that dietary supplementation with selenium may be beneficial in the clinical management of disorders of iron metabolism.
Bartfay
Wally J
WJ
School of Nursing, Queen's University.
Bartfay
Emma
E
D000818:Animals; D009202:Cardiomyopathies / Q000139:chemically induced / Q000188:drug therapy / Q000201:enzymology / Q000378:metabolism*; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005979:Glutathione Peroxidase / Q000378:metabolism*; D019190:Iron Overload / Q000150:complications / Q000188:drug therapy / Q000201:enzymology / Q000378:metabolism*; D008297:Male; D051379:Mice; D008817:Mice, Mutant Strains; D009206:Myocardium / Q000378:metabolism*; D015399:Nursing Research; D011897:Random Allocation; D012643:Selenium / Q000008:administration & dosage / Q000172:deficiency*
D005979:Glutathione Peroxidase; D012643:Selenium