Abstract

Finding a good and long lasting mitigating approach against ionizing radiation is a continuous challenge. Pyruvate or tocopherol derivatives have been chosen for their low toxicity to confirm their intrinsic mitigating properties on L929 mouse fibroblasts against radiation damages up to 72 hours after exposures using colony forming unit assays.60Hz magnetic fields (EMF) interact with cells through the induced electrical field Eind at the membrane surface. In our theoretical model, Eind produces a counter-ion migration from within the Debye layer resulting into a potential change of the membrane surface capable to activate cell signaling such as stress responses. EMF mitigation is presently observed but decreases with time after radiation exposures. To mimic EMF, changing transiently the intracellular redox potential with 100 microM ferricyanide increased strongly cell survival after lethal radiation. 0.1 to 4 Gauss EMF up to 4 hours with mitigating chemical agents are shown to promote cell survival, increasing the equivalent dose ratio from 1.25 (no EMF) to around 2 (with EMF) for pyruvate derivatives.After UVC or X-rays, cells stop within their cell cycle for repair transiently cumulating in G2/M phase. Cells are subject to two different programmed death pathways: apoptosis (G2/M phase) and autophagy (G1, S phases). Flow cytometry shows EMF stimulation unlocking the G2/M blockage towards a transient S phase accumulation. Redox changes with tocopherol or ferricyanide or increases of the ATP energetic pool with pyruvate will suppress autophagy allowing for DNA and cell repairs and completion of cell cycles for cell proliferation.This process of unlocking the cell cycle with EMF to optimizing the effect of the topical treatment has previously been shown increase drug chemotoxicity (taxol, DiHydroArtemisinin, …) in tumor cell lines.

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