Effects of combined radiofrequency field exposure on amyloid-beta-induced cytotoxicity in HT22 mouse hippocampal neurones.
Alzheimer's disease (AD) is the most common progressive and irreversible neurodegenerative disease and it is caused by neuronal death in the brain. Recent studies have shown that non-ionizing radiofrequency (RF) radiation has some beneficial cognitive effects in animal models of AD. In this study, we examined the effect of combined RF radiation on amyloid-beta (Aβ)-induced cytotoxicity in HT22 rat hippocampal neurons. Treatment with Aβ suppressed HT22 cell proliferation in a concentration-dependent manner. RF exposure did not affect cell proliferation, and also had a marginal effect on Aβ-induced suppression of growth in HT22 cells. Cell cycle analysis showed that Aβ decreased the G1 fraction and increased the subG1 fraction, indicating increased apoptosis. Accordingly, Aβ increased the annexin V/propidium iodide (PI)-positive cell fraction and the degradation of poly (ADP ribose) polymerase and caspase-3 in HT22 cells. However, RF alone and the combination of Aβ and RF did not affect these events significantly. Aβ increased reactive oxygen species (ROS) generation, thereby suppressing cell proliferation. This was abrogated by N-acetylcysteine (NAC) treatment, indicating that Aβ-induced ROS generation is the main cause of suppression of proliferation. NAC also restored Aβ-induced annexin V/PI-positive cell populations. However, RF did not have a significant impact on these events. Finally, Aβ stimulated the ataxia telangiectasia and Rad3-related protein/checkpoint kinase 1 DNA single-strand breakage pathway, and enhanced beta-site amyloid precursor protein expression; RF had no effect on them. Taken together, our results demonstrate that RF exposure did not significantly affect the Aβ-induced decrease of cell proliferation, increase of ROS production, or induction of cell death in these cells.
Division of Radiation Cancer Research, Research Center for Radio-Senescence, Korea Institute of Radiological and Medical Sciences, Nowongil 75, Nowon-Gu, Seoul 139-706, Korea.
Jong-Sun
JS
Lee
Division of Radiation Cancer Research, Research Center for Radio-Senescence, Korea Institute of Radiological and Medical Sciences, Nowongil 75, Nowon-Gu, Seoul 139-706, Korea.|Department of Pathology, College of Medicine, Korea University, Seoul 136-705, Korea.
Jeong-Yub
JY
Kim
Division of Radiation Cancer Research, Research Center for Radio-Senescence, Korea Institute of Radiological and Medical Sciences, Nowongil 75, Nowon-Gu, Seoul 139-706, Korea.
Hee-Jin
HJ
Kim
Division of Radiation Cancer Research, Research Center for Radio-Senescence, Korea Institute of Radiological and Medical Sciences, Nowongil 75, Nowon-Gu, Seoul 139-706, Korea.
Jeong Cheol
JC
Kim
Division of Biomedical Sciences, College of Medicine, Inha University, Incheon 400-712, Korea.
Jae-Seon
JS
Lee
School of Information and Communication Engineering, Chungbuk National University, Cheongju 362-763, Korea.
Nam
N
Kim
Division of Radiation Cancer Research, Research Center for Radio-Senescence, Korea Institute of Radiological and Medical Sciences, Nowongil 75, Nowon-Gu, Seoul 139-706, Korea mjpark@kcch.re.kr.
Myung-Jin
MJ
Park
D000111:Acetylcysteine / Q000737:chemistry; D016229:Amyloid beta-Peptides / Q000009:adverse effects*; D000818:Animals; D017209:Apoptosis; D002453:Cell Cycle; D002460:Cell Line; D049109:Cell Proliferation; D002470:Cell Survival / Q000528:radiation effects; D004247:DNA / Q000737:chemistry; D004307:Dose-Response Relationship, Radiation; D005978:Glutathione / Q000378:metabolism; D006624:Hippocampus / Q000166:cytology* / Q000528:radiation effects; D051379:Mice; D009474:Neurons / Q000378:metabolism / Q000528:radiation effects*; D018384:Oxidative Stress; D011829:Radiation Dosage; D011846:Radio Waves; D017382:Reactive Oxygen Species / Q000378:metabolism
D016229:Amyloid beta-Peptides; D017382:Reactive Oxygen Species; D004247:DNA; D005978:Glutathione; D000111:Acetylcysteine
Alzheimer's disease; HT22 hippocampal neuronal cells; amyloid-beta; radiofrequency fields