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Ionising radiation induces persistent alterations in the cardiac mitochondrial function of C57BL/6 mice 40 weeks
Zarko Barjaktarovic1, Alena Shyla, Omid Azimzadeh
1Institute of Radiation Biology, German Research Center for Environmental Health, Neuherberg, Germany. zarko.barjaktarovic@helmholtz-muenchen.de
Background And Purpose:
Radiotherapy of thoracic and chest-wall tumours increases the long-term risk of radiation-induced heart disease. The aim of this study was to investigate the long-term effect of local heart irradiation on cardiac mitochondria.
Methods:
C57BL/6 and atherosclerosis-prone ApoE(-/-) mice received local heart irradiation with a single X-ray dose of 2 Gy. To investigate the low-dose effect, C57BL/6 mice also received a single heart dose of 0.2 Gy. Functional and proteomic alterations of cardiac mitochondria were evaluated after 40 weeks, compared to age-matched controls.
Results:
The respiratory capacity of irradiated C57BL/6 cardiac mitochondria was significantly reduced at 40 weeks. In parallel, protein carbonylation was increased, suggesting enhanced oxidative stress. Considerable alterations were found in the levels of proteins of mitochondria-associated cytoskeleton, respiratory chain, ion transport and lipid metabolism. Radiation induced similar but less pronounced effects in the mitochondrial proteome of ApoE(-/-) mice. In ApoE(-/-), no significant change was observed in mitochondrial respiration or protein carbonylation. The dose of 0.2 Gy had no significant effects on cardiac mitochondria.
Conclusion:
This study suggests that ionising radiation causes non-transient alterations in cardiac mitochondria, resulting in oxidative stress that may ultimately lead to malfunctioning of the heart muscle.
