Jeong-Yub Kim1,2, Hee-Jin Kim1, Nam Kim3, Jong Hwa Kwon4, Myung-Jin Park1. 1. a Korea Institute of Radiological and Medical Sciences , Seoul , Korea. 2. b Department of Pathology , College of Medicine, Korea University , Seoul , Korea. 3. c School of Information and Communication Engineering , Chungbuk National University , Cheongju , Korea. 4. d Department of Radio Technology Research , Electronics and Telecommunications Research Institute , Daejeon , Korea.
Abstract
PURPOSE: To define the impact of radiofrequency (RF) under in vitro experimental Alzheimer's disease conditions, we investigated the effect of RF radiation on glutamate-induced oxidative stress in mouse hippocampal neuronal HT22 cells. MATERIALS AND METHODS: Cell survival rate was measured by MTT and trypan blue exclusion assays. Cell cycle distribution, cell death, and ROS production were analyzed using flow cytometry. Expression of proteins was analyzed by Western blot. RESULTS: RF exposure alone had a marginal impact on cell proliferation; however, it significantly enhanced glutamate-induced cytotoxicity in HT22 cells. Glutamate augmented the subG1 fraction of cell cycle, annexin/propidium iodide positive cell population, and expression of cleaved poly (ADP ribose) polymerase, which were further increased by RF exposure. Glutamate induced reactive oxygen species (ROS) generation and RF exposure further upregulated it. N-acetylcysteine (NAC) treatment completely abrogated glutamate- and RF-induced ROS production followed by cell death and restored cell proliferation in HT22 cells. Finally, glutamate phosphorylated c-Jun N-terminal kinase (JNK) and RF increased this event further. Treatment with NAC and inhibitor of JNK decreased JNK phosphorylation and restored cell proliferation, respectively. CONCLUSIONS: Our results demonstrate that RF exposure enhanced glutamate-induced cytotoxicity by further increase of ROS production in HT22 cells.
PURPOSE: To define the impact of radiofrequency (RF) under in vitro experimental Alzheimer's disease conditions, we investigated the effect of RF radiation on glutamate-induced oxidative stress in mouse hippocampal neuronal HT22 cells. MATERIALS AND METHODS: Cell survival rate was measured by MTT and trypan blue exclusion assays. Cell cycle distribution, cell death, and ROS production were analyzed using flow cytometry. Expression of proteins was analyzed by Western blot. RESULTS:RF exposure alone had a marginal impact on cell proliferation; however, it significantly enhanced glutamate-induced cytotoxicity in HT22 cells. Glutamate augmented the subG1 fraction of cell cycle, annexin/propidium iodide positive cell population, and expression of cleaved poly (ADP ribose) polymerase, which were further increased by RF exposure. Glutamate induced reactive oxygen species (ROS) generation and RF exposure further upregulated it. N-acetylcysteine (NAC) treatment completely abrogated glutamate- and RF-induced ROS production followed by cell death and restored cell proliferation in HT22 cells. Finally, glutamate phosphorylated c-Jun N-terminal kinase (JNK) and RF increased this event further. Treatment with NAC and inhibitor of JNK decreased JNK phosphorylation and restored cell proliferation, respectively. CONCLUSIONS: Our results demonstrate that RF exposure enhanced glutamate-induced cytotoxicity by further increase of ROS production in HT22 cells.
Entities:
Keywords:
Alzheimer’s disease; HT22 hippocampal neuronal cells; glutamate; radiofrequency field