This review summarizes the mechanisms of anthracycline cytotoxicity and side effects such as cardiomyopathy, focusing on oxidative stress and apoptosis.
Reinforces cardiomyopathy monitoring in anthracycline therapy; leaves open mechanism-targeted prevention strategies pending prospective trials.
Anthracycline-derivatives are frequently used chemotherapeutics in treatment of numerous human malignancies. Anthracyclines are known for their complex cytotoxic mechanism involving i) inhibition of enzymes such as topoisomerase II, RNA polymerase, cytochrome c oxidase and others; ii) intercalation into DNA; iii) chelation of iron and generation of reactive oxygen species (ROS); iv) induction of apoptosis. Here, mechanistic aspects for successful cytostasis and for side effects, e.g. cardiomyopathy, are discussed. We emphasize recent developments in anthracycline-mediated apoptosis and focus on a well known representative, doxorubicin (adriamycin, adriblastin). We reflect on the role of oxidative stress and interactions with intracellular signaling pathways.
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Müller et al. (1998) studied this question.
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