Magnetic fields (MFs) are receiving much attention in basic research due to their emerging ability to alter intracellular signaling. We show here that static MFs with intensity of 6 mT significantly alter the intracellular redox balance of U937 cells. A strong increase of reactive oxygen species (ROS) and a decrease of glutathione (GSH) intracellular levels were found after 2 h of MF exposure and maintained thereafter. We found that also other types of MFs, such as extremely-low-frequency (ELF) MFs affect intracellular GSH starting from a threshold at 0.09 mT. We previously reported that static MFs in the intensity range of 0.3-60 mT reduce apoptosis induced by damaging agents (Fanelli et al., 1998). Here, we show that ELF-MFs are also able to protect U937 from apoptosis. Interestingly, this ability is limited to the ELF intensities able to alter redox equilibrium, indicating a link between MF's antiapoptotic effect and the MF alteration of intracellular redox balance. This suggests that MF-produced redox alterations may be part of the signaling pathway leading to apoptosis antagonism. Thus, we tested whether MFs may still exert an antiapoptotic action in cells where the redox state was artificially altered in both directions, that is, by creating an oxidative (via GSH depletion with BSO) or a reducing (with DTT) cellular environment. In both instances, MFs fail to affect apoptosis. Thus, a correct intracellular redox state is required in order for MFs to exert their antiapoptotic effect.

DE NICOLA, M., Cordisco, S., Cerella, C., Albertini, M., D'Alessio, M., Accorsi, A., et al. (2006). Magnetic fields protect from apoptosis via redox alteration. ANNALS OF THE NEW YORK ACADEMY OF SCIENCES, 1090, 59-68 [10.1196/annals.1378.006].

Magnetic fields protect from apoptosis via redox alteration

DE NICOLA, MILENA;BERGAMASCHI, ANTONIO;MAGRINI, ANDREA;GHIBELLI, LINA
2006-12-01

Abstract

Magnetic fields (MFs) are receiving much attention in basic research due to their emerging ability to alter intracellular signaling. We show here that static MFs with intensity of 6 mT significantly alter the intracellular redox balance of U937 cells. A strong increase of reactive oxygen species (ROS) and a decrease of glutathione (GSH) intracellular levels were found after 2 h of MF exposure and maintained thereafter. We found that also other types of MFs, such as extremely-low-frequency (ELF) MFs affect intracellular GSH starting from a threshold at 0.09 mT. We previously reported that static MFs in the intensity range of 0.3-60 mT reduce apoptosis induced by damaging agents (Fanelli et al., 1998). Here, we show that ELF-MFs are also able to protect U937 from apoptosis. Interestingly, this ability is limited to the ELF intensities able to alter redox equilibrium, indicating a link between MF's antiapoptotic effect and the MF alteration of intracellular redox balance. This suggests that MF-produced redox alterations may be part of the signaling pathway leading to apoptosis antagonism. Thus, we tested whether MFs may still exert an antiapoptotic action in cells where the redox state was artificially altered in both directions, that is, by creating an oxidative (via GSH depletion with BSO) or a reducing (with DTT) cellular environment. In both instances, MFs fail to affect apoptosis. Thus, a correct intracellular redox state is required in order for MFs to exert their antiapoptotic effect.
dic-2006
Pubblicato
Rilevanza internazionale
Articolo
Sì, ma tipo non specificato
Settore MED/44 - MEDICINA DEL LAVORO
English
Con Impact Factor ISI
Oxidation-Reduction; Magnetics; Apoptosis; Glutathione; Humans; Reactive Oxygen Species; U937 Cells
DE NICOLA, M., Cordisco, S., Cerella, C., Albertini, M., D'Alessio, M., Accorsi, A., et al. (2006). Magnetic fields protect from apoptosis via redox alteration. ANNALS OF THE NEW YORK ACADEMY OF SCIENCES, 1090, 59-68 [10.1196/annals.1378.006].
DE NICOLA, M; Cordisco, S; Cerella, C; Albertini, M; D'Alessio, M; Accorsi, A; Bergamaschi, A; Magrini, A; Ghibelli, L
Articolo su rivista
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/66728
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 46
  • ???jsp.display-item.citation.isi??? 40
social impact