Iron overload cardiomyopathy is the most prevalent cause of death due to heart failure in young patients in their second and third decades of life. Although the exact mechanism for heart failure is not known, it is hypothesized that a disordered redox balance, such as in selenium deficiency, ultimately leads to free radical mediated damage in a variety of disorders including hemochromatosis. We report here on the effects of selenium and morin hydrate on heart tissue concentrations of iron, glutathione peroxidase activity, and the production of 20 separate aldehyde-derived peroxidation products, in a murine model of chronic iron overload. Sixty B6D2F1 mice were randomized to one of the following four treatment groups for a total period of 4 weeks: (1) control (normal saline, 0.5 ml i.p./ mouse / day); (2) iron-only (iron-dextran, 10 mg i.p. / mouse / day); (3) selenium (sodium selenite, 0.5 ppm orally) and iron, and (4) morin hydrate (0.15 mg i.p./ mouse / day) and iron. Our findings show that supplementation with selenium (sodium selenite) or morin hydrate can decrease, in comparison to iron-only treated groups, both the concentrations of total iron and cytotoxic aldehydes in heart tissue, despite concurrent chronic iron loading in a murine model. Iron and selenium supplemented mice also had significant increases in heart glutathione peroxidase activity, in comparison to iron-only treated mice. This is the first description on the effects of selenium and morin hydrate on the concentrations of iron and cytotoxic aldehydes in heart tissue of a murine model of chronic iron overload. J. Trace Elem. Exp. Med. 13:285–297, 2000. © 2000 Wiley-Liss, Inc.
W. Bartfay, D. Hou, D. Lehotay
Journal of Trace Elements in Experimental Medicine