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

Abstract

Overview

Mitochondria play a pivotal role as the central energy generators in the heart, responsible for producing adenosine triphosphate (ATP) via the oxidative phosphorylation (OXPHOS) system. This study probes how prolonged exposure to electromagnetic fields (EMFs) impacts the mitochondrial OXPHOS system and the structure of the myocardium.

Methods

• Use of 915 MHz EMFs exposure for 28 days on mice to induce electromagnetic stress.
• Measurement tools included Seahorse XF24 analyzer for assessing mitochondrial respiratory function.

Findings

The study revealed significant changes in mitochondrial OXPHOS capacity in mice exposed to EMF, indicating alterations in cardiac protein expression of Complex I, II, III, IV, while the α-subunit of ATP synthase remained stable. Additionally, there were no marked changes in oxidative stress indicators or myocardial expression of antioxidants among the exposed group compared to controls. Structural and functional examinations of left ventricles showed no abnormalities due to electromagnetic stress.

Discussion

Data from this study suggest that prolonged exposure to EMFs could notably affect mitochondrial oxidative metabolism by modulating the cardiac OXPHOS system, thereby impacting the cardiovascular system’s ability to respond to environmental stressors without direct evidence of oxidative or structural damage.

Conclusion

This investigation underscores the potential for EMF exposure to dynamically alter metabolic oxidative status in the myocardium, thus contributing to our understanding of cardiac cell biology under electromagnetic stress conditions, with implications for both health risks and biological adaptations.