Short commentary
Ibrahim El Sayed
Abstract
Doxorubicin, also known as hydroxydaunorubicin, is an anthracycline antibiotic, its structure is closely related to the natural product daunomycin, and like all anthracyclines, works by inhibiting DNA replication. Doxorubicin is very beneficial in treatment of different types of cancer such as liver or breast cancer, its importance is unquestionable in arresting the size of tumor but its cardio toxicity limits its usefulness. There are different mechanisms involved in its cardio toxicity such as the release of free radicals, apoptosis, necrosis and autophagy of cardio myocytes. Doxorubicin-induced heart damage may be due to an increase in cardiac oxidative stress, as indicated by Reactive Oxygen Species (ROS) induced damage such as lipid peroxidation, along with reduced levels of antioxidants and mercapto groups (SH). It was found that irregularities in myofibrillar and intracellular calcium are also important mechanisms for doxorubicin-induced cardiac toxicity. There are at least two targets for doxorubicin-induced apoptosis; it was found that cardiac cells and endothelial cells are affected by doxorubicin-induced apoptosis, as evidenced by caspase activation and internucleosomal DNA damage. Additionally, the changes in the high-energy phosphate pool, endothelin-1 levels, and disturbances of myocardial adrenergic signaling are the most suggested causing factors of cardiac toxicity associated with doxorubicin administration. Therefore, there are different trials aiming to suppress its cardio toxicity to widen its use. Here, in this abstract, we discussed that how much the use of captopril, omega 3 and rosuvastatin could reduce the doxorubicin induced cardio toxicity.