Ilhan Atilla, Gurel Ahmet, Armutcu Ferah, Kamisli Suat, Iraz Mustafa, Akyol Omer, Ozen Suleyman
Department of Neurology, Inonu University, Turgut Ozal Medical Center, 44069 Malatya, Turkey.
Clin Chim Acta. 2004 Feb;340(1-2):153-62. doi: 10.1016/j.cccn.2003.10.012.
The widespread use of mobile phones (MP) in recent years has raised the research activities in many countries to determine the consequences of exposure to the low-intensity electromagnetic radiation (EMR) of mobile phones. Since several experimental studies suggest a role of reactive oxygen species (ROS) in EMR-induced oxidative damage in tissues, in this study, we investigated the effect of Ginkgo biloba (Gb) on MP-induced oxidative damage in brain tissue of rats.
Rats (EMR+) were exposed to 900 MHz EMR from MP for 7 days (1 h/day). In the EMR+Gb groups, rats were exposed to EMR and pretreated with Gb. Control and Gb-administrated groups were produced by turning off the mobile phone while the animals were in the same exposure conditions. Subsequently, oxidative stress markers and pathological changes in brain tissue were examined for each groups.
Oxidative damage was evident by the: (i) increase in malondialdehyde (MDA) and nitric oxide (NO) levels in brain tissue, (ii) decrease in brain superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and (iii) increase in brain xanthine oxidase (XO) and adenosine deaminase (ADA) activities. These alterations were prevented by Gb treatment. Furthermore, Gb prevented the MP-induced cellular injury in brain tissue histopathologically.
Reactive oxygen species may play a role in the mechanism that has been proposed to explain the biological side effects of MP, and Gb prevents the MP-induced oxidative stress to preserve antioxidant enzymes activity in brain tissue.
近年来，手机的广泛使用促使许多国家开展研究活动，以确定暴露于手机低强度电磁辐射（EMR）的后果。由于多项实验研究表明活性氧（ROS）在EMR诱导的组织氧化损伤中起作用，因此在本研究中，我们调查了银杏（Gb）对大鼠脑组织中手机诱导的氧化损伤的影响。
大鼠（EMR+组）暴露于来自手机的900 MHz EMR下7天（每天1小时）。在EMR+Gb组中，大鼠暴露于EMR并预先用Gb处理。对照组和给予Gb的组是在动物处于相同暴露条件下时关闭手机产生的。随后，检查每组脑组织中的氧化应激标志物和病理变化。
氧化损伤表现为：（i）脑组织中丙二醛（MDA）和一氧化氮（NO）水平升高；（ii）脑超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）活性降低；（iii）脑黄嘌呤氧化酶（XO）和腺苷脱氨酶（ADA）活性增加。Gb处理可防止这些改变。此外，Gb在组织病理学上预防了手机诱导的脑组织细胞损伤。
活性氧可能在已提出的解释手机生物学副作用的机制中起作用，并且Gb可防止手机诱导的氧化应激，以维持脑组织中抗氧化酶的活性。
