By Giovanni Luca Beretta, Franco Zunino (auth.), Karsten Krohn (eds.)
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Additional info for Anthracycline Chemistry and Biology II: Mode of Action, Clinical Aspects and New Drugs
1B). In cell-free systems or isolated rat heart preparations these metabolites may be ∼30–40 times more potent than their parent anthracyclines at inactivating ATP-dependent Ca2+ -handling proteins [28–30]; DOXOL is also more potent than DOX at suppressing the gene expression of RyR2 . Perhaps more importantly, secondary alcohol metabolites exhibited a unique reactivity toward the Fe-S cluster of cytoplasmic aconitase/Iron Regulatory Protein-1, an important and versatile regulator of iron homeostasis, energy metabolism, and redox balance of the cell [22, 32, 33].
Attempts to eliminate an involvement of DOXOL in cardiotoxicity formed the rationale to design C-13 deoxydoxorubicin (Fig. 3). When probed in a rabbit chronic model of cardiotoxicity C-13 deoxydoxorubicin caused essentially no effect on major indices of myocardial contractility nor did it suppress the expression of RyR2 . The next logical step was to design an anthracycline (5-imino, C-13 deoxydoxorubicin, provisionally referred to as DIDOX), in which also the quinone moiety had been modiﬁed to eliminate the formation of ROS (Fig.
4 Translating the Metabolic Determinants of Cardiotoxicity into Protective Strategies Antioxidants . . . . . . . . . Iron Chelators . . . . . . . . Noncardiotoxic Anthracycline Analogs . Modulators of Anthracycline Degradation . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 Cardiotoxic Synergism of Anthracyclines with Other Drugs . . . . Anthracyclines and Taxanes . . . . . . . . . .