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 (A beta)-induced cytotoxicity in HT22 rat hippocampal neurons. Treatment with A beta suppressed HT22 cell proliferation in a concentration-dependent manner. RF exposure did not affect cell proliferation, and also had a marginal effect on A beta-induced suppression of growth in HT22 cells. Cell cycle analysis showed that A beta decreased the G1 fraction and increased the subG1 fraction, indicating increased apoptosis. Accordingly, A beta 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 A beta and RF did not affect these events significantly. A beta increased reactive oxygen species (ROS) generation, thereby suppressing cell proliferation. This was abrogated by N-acetylcysteine (NAC) treatment, indicating that A beta-induced ROS generation is the main cause of suppression of proliferation. NAC also restored A beta-induced annexin V/PI-positive cell populations. However, RF did not have a significant impact on these events. Finally, A beta 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 A beta-induced decrease of cell proliferation, increase of ROS production, or induction of cell death in these cells.