Journal
BIOELECTROMAGNETICS
Volume 32, Issue 2, Pages 94-101Publisher
WILEY
DOI: 10.1002/bem.20617
Keywords
mitochondria-deficient cells; DNA double-strand break repair-deficient cells; CD59 mutation
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Funding
- National Nature Science Foundation of China [30570442]
- Foundation of President of the Hefei Institutes of Physical Sciences
- Chinese Academy of Sciences (CAS)
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The literature on the impact of strong static magnetic fields (SMF) on human health is vast and contradictory. The present study focused on the cellular effects of strong homogeneous SMF in human-hamster hybrid (A(L)) cells, mitochondria-deficient (rho(0) A(L)) cells, and double-strand break (DSB) repair-deficient (XRS-5) cells. Adenosine triphosphate (ATP) content was significantly decreased in A(L) cells exposed to 8.5 Tesla (T) but not 1 or 4 T SMF for either 3 or 5 h. In addition, ATP content significantly decreased in the two deficient cell lines exposed to 8.5 TSMF for 3 h. With further incubation of 12 or 24 h without SMF exposure, ATP content could retrieve to the control level in the A(L) cells but not rho(0) A(L) and XRS-5 cells. Under a fluorescence reader, the levels of reactive oxygen species (ROS) in the three cell lines were significantly increased by exposure to 8.5 T SMF for 3 h. Concurrent treatment with ROS inhibitor, DMSO, dramatically suppressed the ATP content in exposed A(L) cells. However, the CD59 mutation frequency and the cell cycle distribution were not significantly affected by exposure to 8.5 T SMF for 3 h. Our results indicated that the cellular ATP content was reduced by 8.5 TSMF for 3 h exposure, which was partially mediated by mitochondria and the DNA DSB repair process. Moreover, ROS were involved in the process of the cellular perturbations from the SMF. Bioelectromagnetics 32: 94-101, 2011. (C) 2010 Wiley-Liss, Inc.
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