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Molecular basis underlying the biological effects elicited by extremely low‐frequency magnetic field (ELF‐MF) on neuroblastoma cells
Author(s) -
Sulpizio Marilisa,
Falone Stefano,
Amicarelli Fernanda,
Marchisio Marco,
Di Giuseppe Fabrizio,
Eleuterio Enrica,
Di Ilio Carmine,
Angelucci Stefania
Publication year - 2011
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.23310
Subject(s) - extremely low frequency , neuroblastoma , basis (linear algebra) , nuclear magnetic resonance , biology , microbiology and biotechnology , physics , magnetic field , cell culture , genetics , mathematics , quantum mechanics , geometry
Extremely low‐frequency magnetic fields (ELF‐MFs) may affect human health because of the possible associations with leukemia but also with cancer, cardiovascular, and neurological disorders. In the present work, human SH‐SY5Y neuroblastoma cells were exposed to a 50 Hz, 1 mT sinusoidal ELF‐MF at three different times, that is, 5 days (T5), 10 days (T10), and 15 days (T15) and then the effects of ELF‐MF on proteome expression and biological behavior were investigated. Through comparative analysis between treated and control samples, we analyzed the proteome changes induced by ELF‐MF exposure. Nine new proteins resolved in sample after a 15‐day treatment were involved in a cellular defense mechanism and/or in cellular organization and proliferation such as peroxiredoxin isoenzymes (2, 3, and 6), 3‐mercaptopyruvate sulfurtransferase, actin cytoplasmatic 2, t‐complex protein subunit beta, ropporin‐1A, and profilin‐2 and spindlin‐1. Our results indicated that ELF‐MFs exposure altered the proliferative status and other important cell biology‐related parameters, such as cell growth pattern, and cytoskeletal organization. These findings support our hypothesis that ELF radiation could trigger a shift toward a more invasive phenotype. J. Cell. Biochem. 112: 3797–3806, 2011. © 2011 Wiley Periodicals, Inc.