Modulation of redox status and calcium handling by extremely low frequency electromagnetic fields in C2C12 muscle cells: A real-time, single-cell approach
The biological effects of electric and magnetic fields, which are ubiquitous in modern society, remain poorly understood. Here, we applied a single-cell approach to study the effects of short-term exposure to extremely low frequency electromagnetic fields (ELF-EMFs) on muscle cell differentiation an...
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Published in: | Free radical biology & medicine Vol. 48; no. 4; pp. 579 - 589 |
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Main Authors: | , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
United States
Elsevier Inc
15-02-2010
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Subjects: | |
Online Access: | Get full text |
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Summary: | The biological effects of electric and magnetic fields, which are ubiquitous in modern society, remain poorly understood. Here, we applied a single-cell approach to study the effects of short-term exposure to extremely low frequency electromagnetic fields (ELF-EMFs) on muscle cell differentiation and function using C2C12 cells as an in vitro model of the skeletal muscle phenotype. Our focus was on markers of oxidative stress and calcium (Ca
2+) handling, two interrelated cellular processes previously shown to be affected by such radiation in other cell models. Collectively, our data reveal that ELF-EMFs (1) induced reactive oxygen species production in myoblasts and myotubes with a concomitant decrease in mitochondrial membrane potential; (2) activated the cellular detoxification system, increasing catalase and glutathione peroxidase activities; and (3) altered intracellular Ca
2+homeostasis, increasing the spontaneous activity of myotubes and enhancing cellular reactivity to a depolarizing agent (KCl) or an agonist (caffeine) of intracellular store Ca
2+channels. In conclusion, our data support a possible link between exposure to ELF-EMFs and modification of the cellular redox state, which could, in turn, increase the level of intracellular Ca
2+and thus modulate the metabolic activity of C2C12 cells. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0891-5849 1873-4596 |
DOI: | 10.1016/j.freeradbiomed.2009.12.005 |