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

Abstract

IntroductionMitochondria are central energy generators for the heart, producing adenosine triphosphate (ATP) through the oxidative phosphorylation (OXPHOS) system. However, mitochondria also guide critical cell decisions and responses to the environmental stressors.MethodsThis study evaluated whether prolonged electromagnetic stress affects the 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.ResultsAnalysis 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 the Seahorse XF24 analyzer demonstrated that prolonged electromagnetic stress modifies the mitochondrial respiratory capacity. However, the plasma level of malondialdehyde, an indicator of oxidative stress, and myocardial expression of mitochondria-resident antioxidant enzyme superoxide dismutase 2 remained unchanged in EMF-exposed mice as compared to controls. At the structural and functional state of left ventricles, no abnormalities were identified in the heart of mice subjected to electromagnetic stress.DiscussionTaken together, these data suggest that prolonged exposure to EMFs could affect mitochondrial oxidative metabolism through modulating cardiac OXPHOS system.

Metabolic, Apoptotic and Fibro-Inflammatory Profiles of the Heart Exposed to Environmental Electromagnetic Fields

“…These contradictory data may be due to the use of different cell models, experimental protocols, and durations of EMF exposure. Indeed, we have recently demonstrated that at the metabolic level, long-term exposure to EMFs could affect mitochondrial oxidative machinery through modulating cardiac OXPHOS capacity in a mouse model [52]. The study indicated that exposure to a 915 EMF for 28 days promotes the cardiac respiratory capacity of mitochondria without compromising the structural integrity of the heart tissues in mice at the age of 9 months.…”

“…Mice were housed in groups of four in polycarbonate cages and were allowed free access to standard food and water. Temperature was controlled at 21 ± 2 • C. Two days before EMF exposure, mice were allowed to adapt to new environmental conditions (light was provided on a 12 h light-12 h dark cycle), as previously described [52]. Animals were randomly divided into two groups: the control sham (n = 10) and EMF (n = 10) groups.…”

The use of NADH anisotropy to investigate mitochondrial cristae alignment

“…It is now clear that electromagnetic fields, such as from rotating magnets, can profoundly influence mitochondrial function, for instance, as an approach to kill cancer cells 53 , or at low intensities (10 µT) and low frequency (1–8 Hz) to induce mitophagy and rejuvenate mitochondrial function 54 . Other data also suggest that prolonged EMF can enhance cardiac and osteogenic mitochondrial function—the proposed mechanism involving a mild production of ROS and possibly complex I involvement 55 , 56 . Interestingly, earlier work showed that magnetic fields could affect the enzyme activity of horseradish catalysed oxidation of NADH.…”

Galanin Coordinates Macrophage-Associated Fibro-Inflammatory Response and Mitochondrial Integrity in Myocardial Infarction Reperfusion Injury

“…Extraction of proteins from cardiac tissues was performed as previously described [ 29 ]. In short, we used RIPA buffer for protein extraction, and the lysates were quantified after clarification using the Bio-Rad Protein Assay (Bio-Rad, Hercules, CA, USA).…”