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ABS TRACT O bjective: Iron-induced cardiotoxicity serves as the main cause of heart failure in young adults and is formidable in many patients. Intracellular iron chelation either by restoring the disturbed cellular iron homeostasis or by removing redox-active iron is the only well-established strategy for cardioprotection. We aimed to evaluate the cardioprotective role of some hydroxypyridine derivative iron chelators on rat myoblast cell line. Material and Methods: Five different derivatives of the 3-hydroxypyridine-4-one scaffold were prepared according a previously reported study. Compounds (10-100 μM) or L1 as standard iron chelator (30-100 μM) dissolved in dimethyl sulfoxide and applied to dulbecco's minimal essential medium (DMEM) culture medium 1 h prior and during H2O2 (100 μM) exposure. H9C2 cells were exposed with FeSO4 (3– 30 μM). Results: Cell survival studies were evaluated through lactate dehydrogenase (LDH) leakage and Annexin-V/ propidium iodide counter staining. Application of iron chelators in the culture media of injured H9C2 cells resulted in non-significant decrease in the amounts of released LDH. Indeed, these compounds were not associated with significant induction of cell death through apoptosis, necrosis or both. Conclusion: The present study demonstrates that these hydroxypyridine derivatives have no effect on nullifying H2O2-induced oxidative stress on in vitro model of cardiac injury.

Cardioprotection Potential of Some Hydroxypyridine Iron Chelators Against H2O2-Induced H9C2 Cell Injury