Low intensity radiofrequency radiation: a new oxidant for living cells
Igor Yakymenko, Evgeniy Sidorik, Diane Henshel, Sergiy Kyrylenko. Editorial. Low intensity radiofrequency radiation: a new oxidant for living cells. Oxid Antioxid Med Sci. 2014; 3(1): 1-3. doi: 10.5455/oams.240314.ed.002.
No abstract
Radiofrequency radiation (RFR), e.g. electromagnetic waves emitted by our cell phones and Wi-Fi, are referred to as non-ionizing. This means that in contrast to the ionizing radiation, which does induce ionization of water and biologically important macromolecules, RFR does not have a capacity for such effects. Unlike, for example X-rays, the energy of RFR is not enough to break electrons off the molecules. However, is RFR completely safe for public health? Traditionally, the industry and the public bodies said yes. Nevertheless, new research data change this perception.
http://www.scopemed.org/?mno=
Open Access Paper: http://www.scopemed.org/
Open Access Paper: http://www.scopemed.org/
Excerpts
Unexpectedly, a strong non-thermal character of biological effects of RFR has been documented. As low as 0.1 μW/cm2 intensity of RFR and absorbed energy (specific absorption rate, SAR) of 0.3 μW/kg were demonstrated to be effective in inducing significant oxidative stress in living cells [27, 29]. This observation is particularly important as the modern international safety limits on RFR exposure are based solely on the thermal effects of the radiation and only restrict RFR intensity to 450-1000 μW/cm2 and SAR to 2 W/kg [30]. Moreover, studies where thermal intensities of RFR have been used could not reveal oxidative effects [31-33], which might point to the variety of molecular mechanisms of action of radiation induced by different radiation intensities.
It is indicative that many studies demonstrated the effectiveness of different antioxidants to reverse the oxidative stress caused by RFR exposure. Such effects have been reported for melatonin [34-37], vitamins E and C [24, 38], caffeic acid phenethyl ester [36], selenium and L-carnitine [39], and garlic extract [40].
It is still a question how low intensity RFR could activate superoxide-generating enzyme NADH oxidase or significantly increase the level of NO in a cell (e.g., possibly due to activation of NO synthase). But what is understood at the moment is that significantly increased levels of ROS in living cells caused by low intensity RFR exposure could lead to mutagenic effects through expressive oxidative damage of DNA [17, 27, 41]. It is also well documented nowadays that in biological systems, oxidants are not necessarily always the triggers for oxidative damage, and that oxidants such as H2O2 could actually serve as signaling messengers and drive several aspects of cellular signaling [42]. This leads to a hypothesis that overproduction of ROS/free radical species in living cells under low intensity RFR exposure can lead to disturbances in cell signaling cascades, which in turn may result in various pathologic consequences.
Unexpectedly, a strong non-thermal character of biological effects of RFR has been documented. As low as 0.1 μW/cm2 intensity of RFR and absorbed energy (specific absorption rate, SAR) of 0.3 μW/kg were demonstrated to be effective in inducing significant oxidative stress in living cells [27, 29]. This observation is particularly important as the modern international safety limits on RFR exposure are based solely on the thermal effects of the radiation and only restrict RFR intensity to 450-1000 μW/cm2 and SAR to 2 W/kg [30]. Moreover, studies where thermal intensities of RFR have been used could not reveal oxidative effects [31-33], which might point to the variety of molecular mechanisms of action of radiation induced by different radiation intensities.
It is indicative that many studies demonstrated the effectiveness of different antioxidants to reverse the oxidative stress caused by RFR exposure. Such effects have been reported for melatonin [34-37], vitamins E and C [24, 38], caffeic acid phenethyl ester [36], selenium and L-carnitine [39], and garlic extract [40].
It is still a question how low intensity RFR could activate superoxide-generating enzyme NADH oxidase or significantly increase the level of NO in a cell (e.g., possibly due to activation of NO synthase). But what is understood at the moment is that significantly increased levels of ROS in living cells caused by low intensity RFR exposure could lead to mutagenic effects through expressive oxidative damage of DNA [17, 27, 41]. It is also well documented nowadays that in biological systems, oxidants are not necessarily always the triggers for oxidative damage, and that oxidants such as H2O2 could actually serve as signaling messengers and drive several aspects of cellular signaling [42]. This leads to a hypothesis that overproduction of ROS/free radical species in living cells under low intensity RFR exposure can lead to disturbances in cell signaling cascades, which in turn may result in various pathologic consequences.
Whatever the particular first-step molecular mechanisms, it is clear that the substantial overproduction of ROS in living cells under low intensity RFR exposure could cause a broad spectrum of health disorders and diseases, including cancer in humans. Undoubtedly, this calls for the further intensive research in the area, as well as to a precautionary approach in routine usage of wireless devices.
--
Joel M. Moskowitz, Ph.D.
Director, Center for Family and Community Health
School of Public Health, University of California, Berkeley
Center: http://cfch.berkeley.edu
Electromagnetic Radiation Safety
Website: http://www.saferemr.com
Facebook: http://www.facebook.com/SaferE
News Releases: http://pressroom.prlog.org/
Twitter: @berkeleyprc
No comments:
Post a Comment