Maskey Dhiraj, Pradhan Jonu, Aryal Bijay, Lee Chang-Min, Choi In-Young, Park Ki-Sup, Kim Seok Bae, Kim Hyung Gun, Kim Myeung Ju
Department of Anatomy, Dankook University College of Medicine, Cheonan, Chungnam, South Korea.
Brain Res. 2010 Jul 30;1346:237-46. doi: 10.1016/j.brainres.2010.05.045. Epub 2010 Jun 17.
Exponential interindividual handling in wireless communication system has raised possible doubts in the biological aspects of radiofrequency (RF) exposure on human brain owing to its close proximity to the mobile phone. In the nervous system, calcium (Ca(2+)) plays a critical role in releasing neurotransmitters, generating action potential and membrane integrity. Alterations in intracellular Ca(2+) concentration trigger aberrant synaptic action or cause neuronal apoptosis, which may exert an influence on the cellular pathology for learning and memory in the hippocampus. Calcium binding proteins like calbindin D28-K (CB) is responsible for the maintaining and controlling Ca(2+) homeostasis. Therefore, in the present study, we investigated the effect of RF exposure on rat hippocampus at 835 MHz with low energy (specific absorption rate: SAR=1.6 W/kg) for 3 months by using both CB and glial fibrillary acidic protein (GFAP) specific antibodies by immunohistochemical method. Decrease in CB immunoreactivity (IR) was noted in exposed (E1.6) group with loss of interneurons and pyramidal cells in CA1 area and loss of granule cells. Also, an overall increase in GFAP IR was observed in the hippocampus of E1.6. By TUNEL assay, apoptotic cells were detected in the CA1, CA3 areas and dentate gyrus of hippocampus, which reflects that chronic RF exposure may affect the cell viability. In addition, the increase of GFAP IR due to RF exposure could be well suited with the feature of reactive astrocytosis, which is an abnormal increase in the number of astrocytes due to the loss of nearby neurons. Chronic RF exposure to the rat brain suggested that the decrease of CB IR accompanying apoptosis and increase of GFAP IR might be morphological parameters in the hippocampus damages.
无线通信系统中的指数个体间处理方式，因其靠近手机，引发了人们对射频（RF）辐射对人脑生物学影响的质疑。在神经系统中，钙（Ca(2+)）在神经递质释放、动作电位产生及膜完整性维持方面发挥着关键作用。细胞内Ca(2+)浓度的改变会引发异常突触活动或导致神经元凋亡，这可能会对海马体中学习和记忆的细胞病理学产生影响。像钙结合蛋白D28-K（CB）这样的钙结合蛋白负责维持和控制Ca(2+)的稳态。因此，在本研究中，我们通过免疫组织化学方法，使用CB和胶质纤维酸性蛋白（GFAP）特异性抗体，研究了835 MHz低能量（比吸收率：SAR = 1.6 W/kg）的RF辐射对大鼠海马体3个月的影响。在暴露组（E1.6）中，CB免疫反应性（IR）降低，CA1区的中间神经元和锥体细胞丢失，颗粒细胞也减少。此外，在E1.6组的海马体中观察到GFAP IR总体增加。通过TUNEL检测，在海马体的CA1、CA3区和齿状回中检测到凋亡细胞，这表明慢性RF辐射可能影响细胞活力。此外，RF辐射导致的GFAP IR增加可能与反应性星形胶质细胞增生的特征相符，反应性星形胶质细胞增生是由于附近神经元丢失导致星形胶质细胞数量异常增加。对大鼠脑的慢性RF辐射表明，伴随凋亡的CB IR降低和GFAP IR增加可能是海马体损伤的形态学参数。
