In this study, dexrazoxane-afforded cardioprotection against chronic anthracycline cardiotoxicity in vivo was evaluated with main focus on a rescue of cardiac myocytes from apoptosis and oxidative stress. The results have shown that DEX-induced protection against chronic ANT cardiotoxicity in vivo is based not only on rescue of cardiomyocytes from necrosis, but also apoptosis.
DEX was shown to block all the major apoptotic pathways triggered by DAU. Moreover, the effective cardioprotection did not appear to be primarily oxidative stress-dependent.