title: Chronic 835-MHz radiofrequency exposure to mice hippocampus alters the distribution of calbindin and GFAP immunoreactivity.
abstract: 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.
authors.affiliation: Department of Anatomy, Dankook University College of Medicine, Cheonan, Chungnam, South Korea.
authors.forename: Dhiraj
authors.initials: D
authors.lastname: Maskey
authors.forename: Jonu
authors.initials: J
authors.lastname: Pradhan
authors.forename: Bijay
authors.initials: B
authors.lastname: Aryal
authors.forename: Chang-Min
authors.initials: CM
authors.lastname: Lee
authors.forename: In-Young
authors.initials: IY
authors.lastname: Choi
authors.forename: Ki-Sup
authors.initials: KS
authors.lastname: Park
authors.forename: Seok Bae
authors.initials: SB
authors.lastname: Kim
authors.forename: Hyung Gun
authors.initials: HG
authors.lastname: Kim
authors.forename: Myeung Ju
authors.initials: MJ
authors.lastname: Kim
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000528:radiation effects; D001253:Astrocytes / Q000528:radiation effects; D064026:Calbindins; D040421:Cell Phone; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism*; D006624:Hippocampus / Q000378:metabolism* / Q000528:radiation effects*; D006706:Homeostasis / Q000528:radiation effects; D007091:Image Processing, Computer-Assisted; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D007395:Interneurons / Q000473:pathology / Q000528:radiation effects; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D017966:Pyramidal Cells / Q000473:pathology / Q000528:radiation effects; D011846:Radio Waves; D064030:S100 Calcium Binding Protein G / Q000378:metabolism*
chemical_list: D064026:Calbindins; D005904:Glial Fibrillary Acidic Protein; D064030:S100 Calcium Binding Protein G