A single-cell approach was applied to study the effects of short-term exposure (30 min) to extremely low frequency electromagnetic fields (50 Hz, 0.1 and 1 mT) on muscle cell differentiation and cell function (the focus was on markers of oxidative stress and calcium handling).
To determine whether intracellular Ca2+ variations were dependent on extracellular Ca2+ influx through voltage-activated calcium channels in the plasma membrane or intracellular Ca2+ release from endoplasmic reticulum/sarcoplasmic reticulum and/or mitochondria via ryanodine-sensitive channels, the authors assessed the effects of extremely low frequency electromagnetic fields on the C2C12 cells in the presence of potassium chloride (a depolarizing agent) or caffeine (an agonist of the ryanodine-sensitive calcium channels).
Exposure duration: continuous for up to 30 min
single cell approach
Exposure duration: continuous for 5 min or 30 min
larger cell samples
Exposure duration: intermittent for 30 min
control for ROS production experiments (field 1)
|Setup||Helmholtz coils with a radius of 445 mm and a distance of 400 mm mounted perpendicular to the ground, located in the working zone of a confocal microscope|
|Additional info||this setup was used for the examination of: i) ROS level ii) membrane potential iii) Ca2+ signaling|
|magnetic flux density||1 mT||-||-||-||-|
The data revealed that extremely low frequency electromagnetic fields 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 enzyme activities; and 3) altered intracellular Ca2+ homeostasis, increasing the spontaneous activity of myotubes and enhancing cellular reactivity to a depolarizing agent (potassium chloride) or an agonist (caffeine) of calcium channels.
The authors conclude that the data support a possible link between exposure to extremely low frequency electromagnetic fields and modification of the cellular redox state, which could, in turn, increase the level of intracellular Ca2+ and thus modulate the metabolic activity of C2C12 cells.