Power Frequency Magnetic Fields Affect the p38 MAPK-Mediated Regulation of NB69 Cell Proliferation Implication of Free Radicals

被引:22
作者
Antonia Martinez, Maria [1 ]
Ubeda, Alejandro [1 ]
Moreno, Jorge [2 ]
Angeles Trillo, Maria [1 ]
机构
[1] Univ Hosp Ramon & Cajal IRYCIS, Serv Invest BEM, Madrid 28034, Spain
[2] UPM, ETSID, Dept Ingn Elect Elect & Automatizac & Fis Aplicad, Madrid 28012, Spain
关键词
extremely low frequency; magnetic field; neuroblastoma; cell cycle; NAC; ERK1/2; JNK; ELECTROMAGNETIC-FIELDS; N-ACETYLCYSTEINE; NEUROBLASTOMA-CELLS; MITOCHONDRIAL ACTIVITY; NITRIC-OXIDE; DNA-DAMAGE; HISTONE H3; CYCLIN D1; GROWTH; EXPOSURE;
D O I
10.3390/ijms17040510
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The proliferative response of the neuroblastoma line NB69 to a 100 mu T, 50 Hz magnetic field (MF) has been shown mediated by activation of the MAPK-ERK1/2 pathway. This work investigates the MF effect on the cell cycle of NB69, the participation of p38 and c-Jun N-terminal (JNK) kinases in the field-induced proliferative response and the potential involvement of reactive oxygen species (ROS) in the activation of the MAPK-ERK1/2 and -p38 signaling pathways. NB69 cultures were exposed to the 100 mu T MF, either intermittently for 24, 42 or 63 h, or continuously for periods of 15 to 120 min, in the presence or absence of p38 or JNK inhibitors: SB203580 and SP600125, respectively. Antioxidant N-acetylcysteine (NAC) was used as ROS scavenger. Field exposure induced transient activation of p38, JNK and ERK1/2. The MF proliferative effect, which was mediated by changes in the cell cycle, was blocked by the p38 inhibitor, but not by the JNK inhibitor. NAC blocked the field effects on cell proliferation and p38 activation, but not those on ERK1/2 activation. The MF-induced proliferative effects are exerted through sequential upregulation of MAPK-p38 and -ERK1/2 activation, and they are likely mediated by a ROS-dependent activation of p38.
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页数:20
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