Cardioprotective effects of selenium and morin hydrate in a murine model of chronic iron overload

Iron overload cardiomyopathy is the most prevalent cause of death due to he art failure in young patients in their second and third decades of life. Al though the exact mechanism for heart failure is not known, it is hypothesiz ed that a disordered redox balance, such as in selenium deficiency, ultimat ely leads to free radical mediated damage in a variety of disorders includi ng hemochromatosis. We report here on the effects of selenium and morin hyd rate on heart tissue concentrations of iron, glutathione peroxidase activit y, and the production of 20 separate aldehyde-derived peroxidation products , in a murine model of chronic iron overload. Sixty B6D2F1 mice were random ized to one of the following four treatment groups for a total period of 4 weeks: (1) control (normal saline, 0.5 mi 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) a nd iron. Our findings show that supplementation with selenium (sodium selen ite) or morin hydrate can decrease, in comparison to iron-only treated grou ps, both the concentrations of total iron and cytotoxic aldehydes in heart tissue, despite concurrent chronic iron lending in a murine model. iron and selenium supplemented mice also had significant increases in heart glutath ione peroxidase activity, in comparison to iron-only treated mice. This is the first description on the effects of selenium and morin hydrate on the c oncentrations of iron and cytotoxic aldehydes in heart tissue of a murine m odel of chronic iron overload. J. Trace Elem. Exp. Med. 13:285-297, 2000. ( C) 2000 Wiley-Liss, Inc.