Abstract

Thermal noise forces and resonance-like responses have presented consistent difficulties in the formulation of mechanistic explanations for weak electromagnetic field (EMF) bioeffects. In many cases, biologically active field strengths appear to lie substantially below the threshold required for electric and magnetic fields to compete directly with thermal forces. It has been suggested1 the thermal threshold for bioeffective electric fields could be as low as 10 μV/cm when tissues (cells with gap junctions) as well as axonal structures are taken into account. Static magnetic field sensitivities in the microTesla (μT) range have been reported for calcium-calmodulin dependent myosin phosphorylation, calmodulin-dependent cyclic nucleotide phosphodiesterase activity in cell-free preparations2,3, as well as at the cellular level4. Many biochemical cascades are regulated by signaling molecules such as calmodulin (CaM) or troponin C, which are in turn regulated by ion binding processes. It has been proposed by one of us that weak EMF bioeffects can occur via modulation of ion dynamics or binding kinetics5. Following this, the magnetic Lorentz force or the Zeeman-Stark effect have been considered6,7, but limitations due to thermal noise and in relating resonance to the charge-to-mass ratio of an unhydrated ion persist.

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