TY - JOUR
T1 - Adaptive response in mouse bone marrow stromal cells exposed to 900 MHz radiofrequency fields
T2 - Impact of poly (ADP-ribose) polymerase (PARP)
AU - He, Qina
AU - Zong, Lin
AU - Sun, Yulong
AU - Vijayalaxmi,
AU - Prihoda, Thomas J.
AU - Tong, Jian
AU - Cao, Yi
N1 - Funding Information:
This research is supported by funding from the National Natural Science Foundation of China (grant# 81373025). The funding agency had no role in designing the experiments, data collection and analysis, preparation of the manuscript, and decision to publish the results. We also thank the technicians in the laboratory for their help during these studies.
Publisher Copyright:
© 2017 Elsevier B.V.
PY - 2017/8
Y1 - 2017/8
N2 - This study examined whether non-ionizing radiofrequency fields (RF) exposure is capable of inducing poly (ADP-ribose) polymerase-1 (PARP-1) in bone marrow stromal cells (BMSCs) and whether it plays a role in RF-induced adaptive response (AR). Bone marrow stromal cells (BMSCs) were exposed to 900 MHz RF at 120 μW/cm2 power flux density for 3 h/day for 5 days and then challenged with a genotoxic dose of 1.5 Gy gamma-radiation (GR). Some cells were also treated with 3-aminobenzamide (3-AB, 2 mM final concentration), a potent inhibitor of PARP-1. Un-exposed and sham (SH)-exposed control cells as well as positive control cells exposed to gamma radiation (GR) were included in the experiments. The expression of PARP-1 mRNA and its protein levels as well as single strand breaks in the DNA and the kinetics of their repair were evaluated at several times after exposures. The results indicated the following. (a) Cells exposed to RF alone showed significantly increased PARP-1 mRNA expression and its protein levels compared with those exposed to SH- and GR alone. (b) Treatment of RF-exposed cells with 3-AB had diminished such increase in PARP-1. (c) Cells exposed to RF + GR showed significantly decreased genetic damage as well as faster kinetics of repair compared with those exposed to GR alone. (d) Cells exposed to RF + 3-AB + GR showed no such decrease in genetic damage. Thus, the overall date suggested that non-ionizing RF exposure was capable of inducing PARP-1 which has a role in RF-induced AR.
AB - This study examined whether non-ionizing radiofrequency fields (RF) exposure is capable of inducing poly (ADP-ribose) polymerase-1 (PARP-1) in bone marrow stromal cells (BMSCs) and whether it plays a role in RF-induced adaptive response (AR). Bone marrow stromal cells (BMSCs) were exposed to 900 MHz RF at 120 μW/cm2 power flux density for 3 h/day for 5 days and then challenged with a genotoxic dose of 1.5 Gy gamma-radiation (GR). Some cells were also treated with 3-aminobenzamide (3-AB, 2 mM final concentration), a potent inhibitor of PARP-1. Un-exposed and sham (SH)-exposed control cells as well as positive control cells exposed to gamma radiation (GR) were included in the experiments. The expression of PARP-1 mRNA and its protein levels as well as single strand breaks in the DNA and the kinetics of their repair were evaluated at several times after exposures. The results indicated the following. (a) Cells exposed to RF alone showed significantly increased PARP-1 mRNA expression and its protein levels compared with those exposed to SH- and GR alone. (b) Treatment of RF-exposed cells with 3-AB had diminished such increase in PARP-1. (c) Cells exposed to RF + GR showed significantly decreased genetic damage as well as faster kinetics of repair compared with those exposed to GR alone. (d) Cells exposed to RF + 3-AB + GR showed no such decrease in genetic damage. Thus, the overall date suggested that non-ionizing RF exposure was capable of inducing PARP-1 which has a role in RF-induced AR.
KW - Adaptive response
KW - DNA damage
KW - Mouse bone marrow stromal cells
KW - Poly (ADP-ribose) polymerase-1
KW - Radiofrequency fields
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U2 - 10.1016/j.mrgentox.2017.05.007
DO - 10.1016/j.mrgentox.2017.05.007
M3 - Article
C2 - 28676262
AN - SCOPUS:85020020809
SN - 1383-5718
VL - 820
SP - 19
EP - 25
JO - Mutation Research - Genetic Toxicology and Environmental Mutagenesis
JF - Mutation Research - Genetic Toxicology and Environmental Mutagenesis
ER -