Adaptive response in mouse bone-marrow stromal cells exposed to 900-MHz radiofrequency fields: Gamma-radiation-induced DNA strand breaks and repair

• Published in: Journal of Toxicology and Environmental Health, Part A Part A, 2016-01, Vol.79 (9-10), p.419-426
• Main Authors: Ji, Yongxin, He, Qina, Sun, Yulong, Tong, Jian, Cao, Yi
• Format: Article
• Language: English
• Subjects: Animals; Bone Marrow Cells - metabolism; Bone Marrow Cells - radiation effects; Break in; Breaking; Comet Assay; Damage; Deoxyribonucleic acid; DNA; DNA Damage; DNA Repair; Eukaryotes; Exposure; Gamma Rays - adverse effects; Histones - metabolism; Male; Mice; Radiation Exposure; Radio Waves - adverse effects; Radiofrequency; Repair; Strands; Stromal Cells - metabolism; Stromal Cells - radiation effects
• ISSN: 1528-7394; 1087-2620; 2381-3504
• DOI: 10.1080/15287394.2016.1176618

The aim of this study was to examine whether radiofrequency field (RF) preexposure induced adaptive responses (AR) in mouse bone-marrow stromal cells (BMSC) and the mechanisms underlying the observed findings. Cells were preexposed to 900-MHz radiofrequency fields (RF) at 120 μW/cm 2 power intensity for 4 h/d for 5 d. Some cells were subjected to 1.5 Gy γ-radiation (GR) 4 h following the last RF exposure. The intensity of strand breaks in the DNA was assessed immediately at 4 h. Subsequently, some BMSC were examined at 30, 60, 90, or 120 min utilizing the alkaline comet assay and γ-H2AX foci technique. Data showed no significant differences in number and intensity of strand breaks in DNA between RF-exposed and control cells. A significant increase in number and intensity of DNA strand breaks was noted in cells exposed to GR exposure alone. RF followed by GR exposure significantly decreased number of strand breaks and resulted in faster kinetics of repair of DNA strand breaks compared to GR alone. Thus, data suggest that RF preexposure protected cells from damage induced by GR. Evidence indicates that in RF-mediated AR more rapid repair kinetics occurs under conditions of GR-induced damage, which may be attributed to diminished DNA strand breakage.