Visit our Expo - Redox and Inflammation signaling 2012

Mechanisms involved in the anti-apoptotic effect of magnetic fields
Maria C. Albertini, Claudia Cerella *, Sonia Cordisco*, Augusto Accorsi, Antonio
Bergamaschi#, Maria D'Alessio*, Milena De Nicola*, Silvia Nuccitelli*, Lina Ghibelli*
Istituto di Chimica Biologica A. Fornaini, Universita' di Urbino, Urbino, Italy
*Dipartimento di Biologia, #Cattedra di Medicina del Lavoro, Universita' di Roma Tor
Vergata, Rome, Italy 00133; *. E-mail: cemetbio@uniurb.it
Concern for possible health hazard due to increasing exposure to magnetic fields (MFs), came
from epidemiological reports indicating a correlation between exposure to MFs and
development of some types of tumors. This led to great interest in the interaction of MFs with
living matter, especially focusing on possible interference on cell metabolism that may
account for a pro-tumoral role of MFs. Research on this issue is made quite difficult since
different types of MFs (i.e., static vs oscillating; different oscillation frequencies; different
intensities; different vector directions; etc.) may differently interact with cells, thus giving rise
to controversial results. We showed that 0.3-60 mTesla (mT) static (i.e., magnete-induced)
MFs may well act as tumor promoting agents, tumor promotion being the epigenetic effect
that allows tumor growth by favoring the growth/survival of transformed cells. Indeed, MFs
strongly reduce the extent of damage-induced apoptosis on a set of cell lines, thus increasing
survival of possibly transformed cells (Fanelli et al., FASEB J 1999, 133:95-102). We
describe here the events triggered by exposure to MFs on a reporter cell line (U937), which
lead to impairment of damage-induced apoptosis, compared to an insensitve one (Jurkat). We
show that MFs anti-apoptotic effect requires a correct redox equilibrium, a working
phospholipase C (PLC, a key actor of receptor-mediated signal transduction), and nitric oxide
syntase (NOS, a key actor of intracellular inflammatory signal transduction), the antiapoptotic
effect being abolished in the presence of reducing (DTT) or oxidizing (BSO)
agents; of PLC inhibitors (neomycin and U73122); and NOS inhibitors (L-NAME),
respectively. Accordingly, the sensitive cells show increased Ca2+ influx, increased IP3
production, plasma membrane hyperpolarization and alterations of free radicals and
glutathione levels. Jurkat cells may be rendered sensitive upon activation with
phytohemagglutinin; the normal/activated Jurkat provide an ideal system where to look for
the primary determinants for the sensitivity to MFs anti-apoptotic effect. Intriguingly,
extremely low frequency (50Hz) electroMFs (ELF) exert similar effects, reducing apoptosis
in a Ca2+ dependent fashion.
LIST OF RECENT PAPERS
Piacentini MP, Piatti E, Fraternale D, Ricci D, Albertini MC, Accorsi A.
Phospholipase C-dependent phosphoinositide breakdown induced by ELF-EMF in Peganum
harmala calli.
Biochimie. 2004 Apr-May;86(4-5):343-9.
Ghibelli L, Teodori L, Cerella C, De Nicola M, D'Alessio M, Clavarino G, Cordisco S,
Albertini MC, Accorsi A, Magrini A, Bergamaschi A.
Epigenetic role of magnetic field exposure in tumor progression: fine-tuning experimental
models]
G Ital Med Lav Ergon. 2003 Jul-Sep;25 Suppl(3):277-8.
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