AUTHOR=Savchenko Lesia , Martinelli Ilenia , Marsal Dimitri , Zhdan Vyacheslav , Tao Junwu , Kunduzova Oksana 

TITLE=Myocardial capacity of mitochondrial oxidative phosphorylation in response to prolonged electromagnetic stress

JOURNAL=Frontiers in Cardiovascular Medicine

VOLUME=Volume 10 - 2023

YEAR=2023

URL=https://www.frontiersin.org/journals/cardiovascular-medicine/articles/10.3389/fcvm.2023.1205893

DOI=10.3389/fcvm.2023.1205893

ISSN=2297-055X

ABSTRACT=Mitochondria are central energy generators for the heart, producing adenosine triphosphate (ATP) through oxidative phosphorylation (OXPHOS) system. However, mitochondria also guide critical cell decisions and responses to the environmental stressors. This study evaluated whether prolonged electromagnetic stress affects mitochondrial OXPHOS system and structural modifications of the myocardium. To induce prolonged electromagnetic stress, mice were exposed to 915 MHz electromagnetic fields (EMFs) for 28 days. Analysis of mitochondrial OXPHOS capacity in EMF-exposed mice pointed to a significant increase in cardiac protein expression of the Complex I, II, III and IV subunits, while expression level of α-subunit of ATP synthase (Complex V) was stable among groups. Furthermore, measurement of respiratory function in isolated cardiac mitochondria using Seahorse XFe24 analyzer demonstrated that prolonged electromagnetic stress modifies mitochondrial respiratory capacity. However, plasma level of malondialdehyde (MDA), an indicator of oxidative stress, and myocardial expression of mitochondria-resident antioxidant enzyme superoxide dismutase 2 (SOD2) remained unchanged in EMF-exposed mice as compared to control. At the structural and functional state of left ventricles, no abnormalities were identified in the heart of mice subjected to electromagnetic stress. Taken together, these data suggest that prolonged exposure to EMFs could affect mitochondrial oxidative metabolism through modulating cardiac OXPHOS system.