Deferiprone does not protect against chronic anthracycline cardiotoxicity in vivo

Abstrakt

This study was focused on the assessment whether novel iron chelator deferiprone (L1) can overcome or significantly reduce the chronic anthracycline cardiotoxicity in the in vivo rabbit model. We revealed that, despite the promising results obtained previously in vitro/ex vivo, iron chelation with L1 was unable to protect the myocardium against lipoperoxidation, cardiomyopathy and heart failure induced by repeated administration of daunorubicin.

Together with our previous findings, this study strongly suggests that the role of iron and its chelation in anthracycline cardiotoxicity is likely not as trivial as originally believed and/or other mechanisms unrelated to iron-catalysed ROS production are involved.