Effects of electromagnetic radiation from a cellular telephone on the oxidant and antioxidant levels in rabbits

• Published in: Cell biochemistry and function Vol. 20; no. 4; pp. 279 - 283
• Main Authors: Irmak, M. Kemal, Fadıllıoğlu, Ersin, Güleç, Mukaddes, Erdoğan, Hasan, Yağmurca, Murat, Akyol, Ömer
• Format: Journal Article
• Language: English
• Published: Chichester, UK John Wiley & Sons, Ltd 01.12.2002
• Subjects: Adenosine Deaminase - metabolism; Animals; antioxidant; Antioxidants - metabolism; Antioxidants - pharmacology; Brain - metabolism; Catalase - metabolism; Cell Phone; cellphone; Free Radicals; Glutathione Peroxidase - metabolism; Male; Malondialdehyde - metabolism; Models, Biological; Nitric Oxide - metabolism; oxidant; Oxidants - metabolism; Peroxidase - metabolism; Rabbits; Radiation; Superoxide Dismutase - metabolism; Xanthine Oxidase - metabolism
• ISSN: 0263-6484; 1099-0844
• DOI: 10.1002/cbf.976

The number of reports on the effects induced by electromagnetic radiation (EMR) in various cellular systems is still increasing. Until now no satisfactory mechanism has been proposed to explain the biological effects of this radiation. Oxygen free radicals may play a role in mechanisms of adverse effects of EMR. This study was undertaken to investigate the influence of electromagnetic radiation of a digital GSM mobile telephone (900 MHz) on oxidant and antioxidant levels in rabbits. Adenosine deaminase, xanthine oxidase, catalase, myeloperoxidase, superoxide dismutase (SOD) and glutathione peroxidase activities as well as nitric oxide (NO) and malondialdehyde levels were measured in sera and brains of EMR‐exposed and sham‐exposed rabbits. Serum SOD activity increased, and serum NO levels decreased in EMR‐exposed animals compared to the sham group. Other parameters were not changed in either group. This finding may indicate the possible role of increased oxidative stress in the pathophysiology of adverse effect of EMR. Decreased NO levels may also suggest a probable role of NO in the adverse effect. Copyright © 2002 John Wiley & Sons, Ltd.