Transferrin delays oxygen radical induced cardiac-contractile failure

Publisher Website
Google Scholar
Abstract
The role of iron-loaded transferrin in xanthine–xanthine oxidase (X–XO) induced cardiac injury in isolated perfused rat hearts was examined. X (2 mM) – XO (10 U/L) perfusion resulted in contractile failure, a rise in resting tension, an increase in lipid peroxidation, and myocardial cell damage. The addition of transferrin (2.4 μM) into the X–XO medium had a protective effect, as indicated by an increase in time to contractile failure, a lesser rise in resting tension, a decrease in MDA values, and lesser damage compared with the X–XO perfused controls. Ultrastructural studies revealed localization of transferrin along the capillary basement membrane. In contrast, addition of transferrin and Desferal (desferrioxamine mesylate, 3 mM, an iron chelator) into X–XO medium caused a rapid contractile failure as well as a rise in resting tension, and in these hearts transferrin was localized inside the myocytes. These findings suggest that a vascular supply of iron protein chelators may have a beneficial effect against myocardial cell injury caused by a vascular source of oxygen radicals.Key words: oxy-radical injury, myocardial failure, lipid peroxidation, heart cell damage, iron binding proteins.