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These events lead to a state of vascular inflammation, which may be partially mediated by ROS formed by activated mononuclear cells

However, the therapeutic utility of doxorubicin is undermined by its dose-dependent cardiotoxicity, possibly arising as a result of futile redox cycling, with NADH dehydrogenase within the mitochondria proposed as the most likely site of anthracycline reduction 9,10

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