Impact of 60‐GHz millimeter waves and corresponding heat effect on endoplasmic reticulum stress sensor gene expression. Issue 6 (6th August 2014)

• Record Type: Journal Article
• Authors: Le Quément, Catherine; Nicolaz, Christophe Nicolas; Habauzit, Denis; Zhadobov, Maxim; Sauleau, Ronan; Le Dréan, Yves
• Is Part Of: Bioelectromagnetics. Volume 35:Issue 6(2014:Sep.)
• Page Start: 444
• Page End: 451
• Publication Date: 2014-08-06
• Subjects: Electromagnetism -- Physiological effect -- Periodicals; 571.47
• DOI: 10.1002/bem.21864
• Languages: English
• ISSNs: 0197-8462

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="bem21864-sec-0001" sec-type="section"> <p>Emerging high data rate wireless communication systems, currently under development, will operate at millimeter waves (MMW) and specifically in the 60 GHz band for broadband short‐range communications. The aim of this study was to investigate potential effects of MMW radiation on the cellular endoplasmic reticulum (ER) stress. Human skin cell lines were exposed at 60.4 GHz, with incident power densities (IPD) ranging between 1 and 20 mW/cm². The upper IPD limits correspond to the ICNIRP local exposure limit for the general public. The expression of ER‐stress sensors, namely <italic>BIP</italic> and <italic>ORP150</italic>, was then examined by real‐time RT‐PCR. Our experimental data demonstrated that MMW radiations do not change <italic>BIP</italic> or <italic>ORP150</italic> mRNA basal levels, whatever the cell line, the exposure duration or the IPD level. Co‐exposure to the well‐known ER‐stress inducer thapsigargin (TG) and MMW were then assessed. Our results show that MMW exposure at 20 mW/cm² inhibits TG‐induced <italic>BIP</italic> and <italic>ORP150</italic> over expression. Experimental controls showed that this inhibition is linked to the thermal effect resulting from the MMW exposure. Bioelectromagnetics. 35:444–451, 2014. © 2014 Wiley Periodicals, Inc.</p> </sec> </abstract>