scholarly journals Oxidative Stress in Radiation-Induced Cardiotoxicity

2020 ◽  
Vol 2020 ◽  
pp. 1-15 ◽  
Author(s):  
Zhang Ping ◽  
Yang Peng ◽  
Hong Lang ◽  
Cai Xinyong ◽  
Zeng Zhiyi ◽  
...  

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.

2021 ◽  
Vol 19 ◽  
Author(s):  
Tapan Behl ◽  
Gagandeep Kaur ◽  
Aayush Sehgal ◽  
Gokhan Zengin ◽  
Sukhbir Singh ◽  
...  

Background: Ionizing radiation from telluric sources is unceasingly an unprotected pitfall to humans. Thus, the foremost contributors to human exposure are global and medical radiations. Various pieces of evidences assembled during preceding years reveal the pertinent role of ionizing radiation-induced oxidative stress in the progression of neurodegenerative insults such as Parkinson’s disease, which have been contributing to increased proliferation and generation of reactive oxygen species. Objective: This review delineates the role of ionizing radiation-induced oxidative stress in Parkinson’s disease and proposes novel therapeutic interventions of flavonoid family offering effective management and slowing down the progression of Parkinson’s disease. Method: Published papers were searched via MEDLINE, PubMed, etc. published to date for in-depth database collection. Results: The potential of oxidative damage may harm the non-targeted cells. It can also modulate the functions of central nervous system, such as protein misfolding, mitochondria dysfunction, increased levels of oxidized lipids, and dopaminergic cell death, which accelerates the progression of Parkinson’s disease at the molecular, cellular, or tissue levels. In Parkinson’s disease, reactive oxygen species exacerbate the production of nitric oxides and superoxides by activated microglia, rendering death of dopaminergic neuronal cell through different mechanisms. Conclusion: Rising interest has extensively engrossed on the clinical trial designs based on the plant derived family of antioxidants. They are known to exert multifarious impact either way in neuroprotection via directly suppressing ionizing radiation-induced oxidative stress and reactive oxygen species production or indirectly increasing the dopamine levels and activating the glial cells.


PLoS ONE ◽  
2009 ◽  
Vol 4 (7) ◽  
pp. e6377 ◽  
Author(s):  
Nicole L. Simone ◽  
Benjamin P. Soule ◽  
David Ly ◽  
Anthony D. Saleh ◽  
Jason E. Savage ◽  
...  

2018 ◽  
Vol 24 (4) ◽  
pp. 340-345 ◽  
Author(s):  
Peyman Amini ◽  
Saeed Rezapoor ◽  
Dheyauldeen Shabeeb ◽  
Ahmed Eleojo Musa ◽  
Masoud Najafi ◽  
...  

Background: Epidemiological studies have shown an increased incidence of heart diseases among survivors of Chernobyl disaster as well as Hiroshima and Nagasaki atomic bomb explosion. Similar results were observed for lung and left breast cancer patients. Experimental studies have proposed the chronic upregulation of some pro-inflammatory and pro-fibrotic cytokines. Recent studies have shown that upregulation of pro-oxidant enzymes play a key role in the development of late effects of ionizing radiation such as fibrosis. Interleukin-4 (IL-4) and Interleukin-13 (IL-13) are two important cytokines that have shown ability to induce production of free radicals through dual oxidases (Duox) i.e. Duox1 and Duox2. In this study, we aimed to detect the expression of IL-4 receptor-a1 (IL-4Ra1), IL-13 receptor-a2 (IL-13Ra2), Duox1 and Duox2 genes following irradiation of rat’s heart. In addition, we evaluated the possible role of the combination of curcumin and selenium-L-methionine on the regulation of these genes. Methods: Twenty rats were divided into 4 groups as follows; G1: control; G2: treatment with the combination of curcumin and selenium-L-methionine; G3: radiation; G4: radiation plus treatment with the combination of curcumin and selenium-L-methionine. Rats were sacrificed 10 weeks after irradiation for detecting the expression of IL-4Ra1, IL-13Ra2, Duox1 and Duox2. Results: Results showed that exposure to ionizing radiation caused upregulation of IL-4Ra1 by more than 4-fold as well as Duox1 and Duox2 by more than 5-fold. However, results showed no detectable expression for IL-13Ra2. Treatment with the combination of curcumin and selenium-L-methionine could attenuate the upregulation of all genes. Conclusion: This study has shown that exposing rat’s heart tissues to radiation leads to chronic upregulation of IL-4Ra1, Duox1 and Duox2 as well as pro-oxidant enzymes. Treatment with the combination of curcumin and selenium-L-methionine showed ability to attenuate the upregulation of these genes.


Toxicology ◽  
2021 ◽  
pp. 307-316
Author(s):  
Tiziana Cervelli ◽  
Giuseppina Basta ◽  
Serena Del Turco

Author(s):  
Marziyeh Raeispour ◽  
Fereshteh Talebpour Amiri ◽  
Soghra Farzipour ◽  
Arash Ghasemi ◽  
Seyed Jalal Hosseinimehr

2018 ◽  
Vol 53 (4) ◽  
pp. 241-248 ◽  
Author(s):  
J.-L. Ravanat

During the last few decades, a considerable amount of work has been done to better assess the effects of ionizing radiation on living organisms. In particular a lot of attention has been focused on the consequences of modifications of the DNA macromolecule, the support of the genetic information. Detailed information is now available on the formation of radiation-induced DNA lesions at the physical, chemical and biological levels. Emphasis will be placed in this review article on the differences and similarities, in term of DNA lesions formation and outcome, between endogenous oxidative stress and ionizing radiation, both stresses that could produce oxidative DNA lesions through similar mechanistic pathways involving mostly reactive oxygen species. If the chemical nature of the generated lesions is similar, the differences in term of biological consequences could be attributed to their spatial distribution in genomic DNA, since ionizing radiations produce lesions in cluster. These clusters of lesions represent a challenge for the DNA repair machinery. In contrast, endogenous oxidative stress generates scattered lesions that could be repaired with a much higher efficacy and fidelity. Possible implication of the use of DNA damage and repair for human health purposes and radiological protection will be discussed.


2019 ◽  
Vol 22 (5) ◽  
pp. 490-498 ◽  
Author(s):  
Hyung Taek Cho ◽  
Jun Ho Kim ◽  
Wan Heo ◽  
Hyun-Sun Lee ◽  
Jeong Jun Lee ◽  
...  

2020 ◽  
Vol 21 (7) ◽  
pp. 2281 ◽  
Author(s):  
Anna Lichota ◽  
Ireneusz Piwoński ◽  
Sylwia Michlewska ◽  
Anita Krokosz

The aim of this study was to investigate the uptake and accumulation of fullerenol C60(OH)36 into peripheral blood mononuclear cells (PBMCs). Some additional studies were also performed: measurement of fullerenol nanoparticle size, zeta potential, and the influence of fullerenol on the ionizing radiation-induced damage to PMBCs. Fullerenol C60(OH)36 demonstrated an ability to accumulate in PBMCs. The accumulation of fullerenol in those cells did not have a significant effect on cell survival, nor on the distribution of phosphatidylserine in the plasma membrane. However, fullerenol-induced depolarization of the mitochondrial membrane proportional to the compound level in the medium was observed. Results also indicated that increased fullerenol level in the medium was associated with its enhanced transport into cells, corresponding to its influence on the mitochondrial membrane. The obtained results clearly showed the ability of C60(OH)36 to enter cells and its effect on PBMC mitochondrial membrane potential. However, we did not observe radioprotective properties of fullerenol under the conditions used in our study.


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