Electromagnetic Fields Act Similarly in Plants as in Animals: Probable Activation of Calcium Channels via Their Voltage Sensor

Title:Electromagnetic Fields Act Similarly in Plants as in Animals: Probable Activation of Calcium Channels via Their Voltage Sensor

Volume: 10 Issue: 1

Author(s): Martin L. Pall

Affiliation:

Keywords: Microwave frequency non-thermal effects, calcium signaling, ion channel evolution, EMFs as an environmental stressor, free radicals including hydroxyl, carbonate and NO₂ radicals.

Abstract: It has been shown that low intensity microwave/lower frequency electromagnetic fields (EMFs) act in animals via activation of voltage-gated calcium channels (VGCCs) in the plasma membrane, producing excessive intracellular calcium [Ca²⁺]i, with excessive [Ca²⁺]i leading to both pathophysiological and also in some cases therapeutic effects. The pathophysiological effects are produced largely through excessive [Ca²⁺]i signaling including excessive nitric oxide (NO), superoxide, peroxynitrite, free radical formation and consequent oxidative stress. The activation of the VGCCs is thought to be produced via EMF impact on the VGCC voltage sensor, with the physical properties of that voltage sensor predicting that it is extraordinarily sensitive to these EMFs. It is shown here that the action of EMFs in terrestrial, multicellular (embryophyte) plants is probably similar to the action in animals in most but not all respects, with calcium channel activation in the plasma membrane leading to excessive [Ca²⁺]i, leading in turn to most if not all of the biological effects. A number of studies in plants are briefly reviewed which are consistent with and supportive of such a mechanism. Plant channels most plausibly to be involved, are the so-called two pore channels (TPCs), which have a voltage sensor similar to those found in the animal VGCCs.

Cite this article as:

Pall L. Martin, Electromagnetic Fields Act Similarly in Plants as in Animals: Probable Activation of Calcium Channels via Their Voltage Sensor, Current Chemical Biology 2016; 10 (1) . https://dx.doi.org/10.2174/2212796810666160419160433