Redox interactions-induced cardiac toxicity in cancer therapy

Abstract

Cancer patients undergoing radiotherapy, chemotherapy, or targeted cancer therapy are exposed to the risk of several side effects because of the heavy production of ROS by ionizing radiation or some chemotherapy drugs. Damages to DNA, mitochondria, membrane and other organelles within normal tissue cells such as cardiomyocytes and endothelial cells lead to the release of some toxins which are associated with triggering inflammatory cells to release several types of cytokines, chemokines, ROS, and RNS. The release of some molecules following radiotherapy or chemotherapy stimulates reduction/oxidation (redox) reactions. Redox reactions cause remarkable changes in the level of reactive oxygen species (ROS) and reactive nitrogen species (RNS). Excessive production of ROS and RNS or suppression of antioxidant defense enzymes leads to damage to critical macromolecules, which may continue for long times. Increased levels of some cytokines and oxidative injury are hallmarks of heart injury following cancer therapy. Redox reactions may be involved in several heart disorders such as fibrosis, cardiomyopathy, and endothelium injury. In the current review, we explain the cellular and molecular mechanisms of redox interactions following radiotherapy, chemotherapy, and targeted cancer therapy. Afterward, we explain the evidence of the involvement of redox reactions in heart diseases.

Keywords: Cancer therapy; Cardiomyopathy; Chemotherapy; Endothelial dysfunction; Heart; Radiotherapy; Redox.