Date Published: February 20, 2018
Publisher: Public Library of Science
Author(s): M. Lasalvia, R. Scrima, G. Perna, C. Piccoli, N. Capitanio, P. F. Biagi, L. Schiavulli, T. Ligonzo, M. Centra, G. Casamassima, A. Ermini, V. Capozzi, Irina V. Lebedeva.
Blood is a fluid connective tissue of human body, where it plays vital functions for the nutrition, defense and well-being of the organism. When circulating in peripheral districts, it is exposed to some physical stresses coming from outside the human body, as electromagnetic fields (EMFs) which can cross the skin. Such fields may interact with biomolecules possibly inducing non thermal-mediated biological effects at the cellular level. In this study, the occurrence of biochemical/biological modifications in human peripheral blood lympho-monocytes exposed in a reverberation chamber for times ranging from 1 to 20 h to EMFs at 1.8 GHz frequency and 200 V/m electric field strength was investigated. Morphological analysis of adherent cells unveiled, in some of these, appearance of an enlarged and deformed shape after EMFs exposure. Raman spectra of the nuclear compartment of cells exposed to EMFs revealed the onset of biochemical modifications, mainly consisting in the reduction of the DNA backbone-linked vibrational modes. Respirometric measurements of mitochondrial activity in intact lympho-monocytes resulted in increase of the resting oxygen consumption rate after 20 h of exposure, which was coupled to a significant increase of the FoF1-ATP synthase-related oxygen consumption. Notably, at lower time-intervals of EMFs exposure (i.e. 5 and 12 h) a large increase of the proton leak-related respiration was observed which, however, recovered at control levels after 20 h exposure. Confocal microscopy analysis of the mitochondrial membrane potential supported the respiratory activities whereas no significant variations in the mitochondrial mass/morphology was observed in EMFs-exposed lympho-monocytes. Finally, altered redox homeostasis was shown in EMFs-exposed lympho-monocytes, which progressed differently in nucleated cellular subsets. This results suggest the occurrence of adaptive mechanisms put in action, likely via redox signaling, to compensate for early impairments of the oxidative phosphorylation system caused by exposure to EMFs. Overall the data presented warn for health safety of people involved in long-term exposure to electromagnetic fields, although further studies are required to pinpoint the leukocyte cellular subset(s) selectively targeted by the EMFs action and the mechanisms by which it is achieved.
The exposure of humans to electromagnetic fields (EMFs) enormously increased during the last century and it is still increasing today as a consequence of the industrial and technical development, which involves generation of artificial EMFs sources (radio and television stations and receivers, radar, computers, Wi-Fi antennas, mobile phones, microwave ovens, and many devices used in medicine and industry). In particular, the exposure to EMFs (from 300 MHz to 300 GHz) is extensively increasing due to the huge use of wireless communications devices working in such a frequency range. The first effect of such exposure consists in the local heating of tissues located inside the penetration depth of radiation (thermal effect), as a consequence of energy transfer from EMFs to the oscillating charges inside the biological tissues. However, the increase of temperature is counteracted by physiological mechanisms of heat dispersion and, therefore, it can be considered as a negligible effect with no dangerous risks involved. The non-thermal-related effects of EMFs on biomolecular structures have been largely investigated in the latest years. Nevertheless, because of controversial and discrepant results, this issue is still object of scientific debate. This subject is still largely investigated, especially by in vitro experiments, where some experimental parameters can be changed and easily controlled.
This work investigates the effects of 1.8 GHz electromagnetic field at the electric field strength of 200 V/m on peripheral blood, focusing the analysis to leukocyte cells isolated from the blood after exposure to 1h, 5h, 12h and 20h times. The physical parameters used in the exposure protocol are within the EMFs values produced by mobile phones at a SAR comparable to the limit values allowed in European countries. Based on the discussed results, it is justified to conclude that the EMFs exposure of microwave radiation may alter the morphology of the lympho-monocyte blood component. Most notably, Raman spectroscopy analysis unveils changes in the biochemical composition of the lympho-monocyte nuclear compartment before the overt appearance of the cellular morphological changes. Such differences mainly consist of a decrease of the DNA and nucleic acid backbone-related signals with respect to those of the proteins, possibly caused by EMFs-induced alteration of the chemical environment surrounding the nucleus. Respirometric analysis of EMFs-exposed PBLM cells, largely constituted by lymphocyte, results in in a biphasic outcome with an earlier impairment of the mitochondrial OxPhos activity followed by an overwhelming recovering. This effect is paralleled by changes in the ΔΨm. No appreciable variations either in the mitochondria mass and morphology is observed ruling out substantial changes in mitochondrial biogenesis or degradation. Nevertheless, a clear alteration of the intracellular redox balance is observed in the EMFs-treated nucleated PBLM preparations at time-point as earlier as 5 h. The impact of EMFs on the cellular ROS level has been object of extensive investigation leading to contrasting results. Multiple factors could cause these discrepancies, including but not limited to EMFs type/intensity/frequency, exposure time and assay time-point, as well as different biological samples examined . The novel finding reported in the presented study would indicate the requirement of a functional nucleus in the cell to elicit the observed EMFs-mediated unbalance of the cellular redox tone since this was absent in the anucleate platelets.