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

Abstract

Myocardial capacity of mitochondrial oxidative phosphorylation in response to prolonged electromagnetic stress Savchenko L, Martinelli I, Marsal D, Zhdan V, Tao J, Kunduzova O. Myocardial capacity of mitochondrial oxidative phosphorylation in response to prolonged electromagnetic stress. Front Cardiovasc Med. 2023 Jun 7;10:1205893. doi: 10.3389/fcvm.2023.1205893. Abstract Introduction: Mitochondria 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. Methods: This 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. Results: 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 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. Discussion: Taken together, these data suggest that prolonged exposure to EMFs could affect mitochondrial oxidative metabolism through modulating cardiac OXPHOS system. Excerpt To induce electromagnetic stress, in vivo experiments were performed in a Giga-TEM (GTEM) cell. For animal adaptation, 24 h prior to tests mice were placed in the GTEM cell. A solid-state radiofrequency generator with a fixed frequency of 915 MHz (WSPS-915–1000) (Chengdu Wattsine Electronics Technology, Chengdu, Sichuan, China) was used for in vivo experiments The estimated specific absorption rate (SAR) values were around 40 W/kg In radio frequency (RF) testing, the input power was 4 W in the high frequency structure simulator (HFSS) simulation and in the experimentation, as previously described (15, 16). Conclusion The ability of cardiac cells to adjust the mitochondrial oxidative metabolism in response to environmental stress is a well-recognized signature of the cardiovascular system. Persistent metabolic changes may result in tissue abnormalities or may trigger cell maladaptive responses. Our study points at notable differences between control and EMF-challenged mice hearts at the level of mitochondrial respiration after prolonged EMF exposure. As the mouse heart imitates the mammalian cardiovascular phenotype, our data suggest that metabolic oxidative status changes dynamically in response to EMFs in the myocardium, challenging our quest to better understand cardiac cell biology under conditions of electromagnetic environment. Open access paper: frontiersin.org

AI evidence extraction

Main findings

Mice exposed to 915 MHz EMFs for 28 days showed increased cardiac protein expression of Complex I–IV subunits, with stable expression of the ATP synthase (Complex V) α-subunit. Mitochondrial respiratory capacity in isolated cardiac mitochondria was modified, while plasma malondialdehyde and myocardial SOD2 were unchanged and no left-ventricle structural/functional abnormalities were identified.

Outcomes measured

• Mitochondrial oxidative phosphorylation (OXPHOS) capacity in myocardium
• Cardiac protein expression of mitochondrial respiratory chain complexes I–V subunits
• Mitochondrial respiratory function (Seahorse XF24)
• Plasma malondialdehyde (oxidative stress marker)
• Myocardial superoxide dismutase 2 (SOD2) expression
• Left ventricle structural and functional abnormalities

Limitations

• Sample size not reported in provided abstract/metadata
• Exposure source/context (e.g., device type, modulation details) not specified beyond GTEM cell and 915 MHz generator
• Findings are from an animal model; human relevance not established in the provided text

Suggested hubs

• rf-animal-studies (0.9)
  Animal experiment exposing mice to 915 MHz RF EMFs and assessing cardiac/mitochondrial outcomes.

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        "sar_wkg": 40,
        "duration": "28 days"
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    "population": "Mice",
    "sample_size": null,
    "outcomes": [
        "Mitochondrial oxidative phosphorylation (OXPHOS) capacity in myocardium",
        "Cardiac protein expression of mitochondrial respiratory chain complexes I–V subunits",
        "Mitochondrial respiratory function (Seahorse XF24)",
        "Plasma malondialdehyde (oxidative stress marker)",
        "Myocardial superoxide dismutase 2 (SOD2) expression",
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    ],
    "main_findings": "Mice exposed to 915 MHz EMFs for 28 days showed increased cardiac protein expression of Complex I–IV subunits, with stable expression of the ATP synthase (Complex V) α-subunit. Mitochondrial respiratory capacity in isolated cardiac mitochondria was modified, while plasma malondialdehyde and myocardial SOD2 were unchanged and no left-ventricle structural/functional abnormalities were identified.",
    "effect_direction": "mixed",
    "limitations": [
        "Sample size not reported in provided abstract/metadata",
        "Exposure source/context (e.g., device type, modulation details) not specified beyond GTEM cell and 915 MHz generator",
        "Findings are from an animal model; human relevance not established in the provided text"
    ],
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    "peer_reviewed_likely": "yes",
    "keywords": [
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        "OXPHOS",
        "respiration",
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        "malondialdehyde",
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