Abstract
There is a distinct increase in the risk of heart disease in people exposed to ionizing radiation (IR). Radiation-induced heart disease (RIHD) is one of the adverse side effects when people are exposed to ionizing radiation. IR may come from various forms, such as diagnostic imaging, radiotherapy for cancer treatment, nuclear disasters, and accidents. However, RIHD was mainly observed after radiotherapy for chest malignant tumors, especially left breast cancer. Radiation therapy (RT) has become one of the main ways to treat all kinds of cancer, which is used to reduce the recurrence of cancer and improve the survival rate of patients. The potential cause of radiation-induced cardiotoxicity is unclear, but it may be relevant to oxidative stress. Oxidative stress, an accumulation of reactive oxygen species (ROS), disrupts intracellular homeostasis through chemical modification and damages proteins, lipids, and DNA; therefore, it results in a series of related pathophysiological changes. The purpose of this review was to summarise the studies of oxidative stress in radiotherapy-induced cardiotoxicity and provide prevention and treatment methods to reduce cardiac damage.
Highlights
Radiotherapy plays an important role in the treatment of many cancers
NF-κB is activated by oxidative stress after radiation, which targets the production of many genes related to inflammation, including intercellular adhesion molecules (ICAM), vascular cell adhesion molecules (VCAM), and cytokines, and promotes the upregulation of thrombus formation markers [40]
The results indicate that melatonin at high concentration was a potential adjuvant in patients with head and neck squamous cell carcinoma who were undergoing radiotherapy [101]
Summary
Radiotherapy plays an important role in the treatment of many cancers. As the use of radiotherapy is becoming increasingly frequent, and since the overall patient survival rate is high, the risks associated with radiotherapy must be carefully considered. NF-κB is activated by oxidative stress after radiation, which targets the production of many genes related to inflammation, including intercellular adhesion molecules (ICAM), vascular cell adhesion molecules (VCAM), and cytokines, and promotes the upregulation of thrombus formation markers [40]. As an antioxidant, may prevent radiation-induced CVD in a variety of ways It inhibits ROS-producing enzymes in mitochondria and reduces the production of free radicals. The level of oxidative stress in the heart of mice fed with hesperidin was significantly decreased, such as the increased expression of antioxidant enzymes, including SOD1 and SOD2, and passivation of NADPH oxidase. It was found that hesperidin could protect the heart of aged rats by mediating the expression of Nrf, upregulating the activity of antioxidant enzymes and reducing the macromolecular damage induced by oxidative stress [98]
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