Iron-overload cardiomyopathy: evidence for a free radical--mediated mechanism of injury and dysfunction in a murine model.

摘要: Iron-overload cardiomyopathy is a restrictive that manifests itself as systolic or diastolic dysfunction secondary to increased deposition of iron in the heart and occurs with common genetic disorders such primary hemochromatosis beta-thalassemia major. Although exact mechanism iron-induced failure remains be elucidated, toxicity biological systems believed attributed its ability catalyze generation oxygen-free radicals. In current investigation, dose-dependent effects chronic iron-loading on tissue concentrations iron, glutathione peroxidase (GPx) activity, free-radical production, cardiac were investigated murine model iron-overload cardiomyopathy. It was shown results (a) increases myocardial burden, (b) decreases protective antioxidant enzyme GPx (c) (d) mortality. These findings show involves part free radical-mediated processes.