Why the study?
Do aroylhydrazone iron chelators prevent daunorubicin-induced cardiotoxicity and mortality in rabbits?
Do aroylhydrazone iron chelators prevent daunorubicin-induced cardiotoxicity and mortality in rabbits?
Aroylhydrazone iron chelators protect against anthracycline-induced cardiotoxicity and mortality in a rabbit model at specific doses, but higher doses may paradoxically worsen outcomes.
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May support dose-specific aroylhydrazone chelation against anthracycline cardiotoxicity in rabbits; hypothesis-generating and leaves open clinical translation.
The risk of cardiotoxicity is the main drawback of anthracycline antibiotics. However, these drugs remain among the most effective and frequently used anti cancer drugs. In this study we aimed to assess the cardioprotective effects of aroylhydrazone iron (FE) chelators: pyridoxal isonicotinoyl hydrazone (PIH) and its two analogs: salicyladehyde isonicotinoyl hydrazone (SIH) and pyridoxal o-chlorbenzoyl hydrazone (o-108). In rabbits, chronic treatment with daunorubicin (DAU) (3 mg/kg weekly for 10 weeks) induced mortality (33%) as well as left ventricular (LV) dysfunction. Co-administrations of PIH (25 mg/kg, i.p.), SIH hydrochloride [1 mg/kg, iv] as well as o-108 (10 mg/kg, i.p.), fully prevented premature deaths and most of the DAU-induced functional impairments were significantly suppressed. However, when 2- to 2.5-fold higher doses of the chelators were used, they led to rather paradoxical and mostly negative results regarding both cardioprotection and overall mortality.
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Šimůnek et al. (2008) studied this question.
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