This study aims to assess whether a 1950 MHz radiofrequency (RF) electromagnetic feld could protect human neuroblastoma SH-SY5Y cells against a subsequent treatment with menadione, a chemical agent inducing DNA damage via reactive oxygen species formation. Cells were pre-exposed for 20h to specifc absorption rate of either 0.3 or 1.25W/kg, and 3h after the end of the exposure, they were treated with 10µM menadione (MD) for 1h. No diferences were observed between sham- and RFexposed samples. A statistically signifcant reduction in menadione-induced DNA damage was detected in cells pre-exposed to either 0.3 or 1.25W/kg (P<0.05). Moreover, our analyses of gene expression revealed that the pre-exposure to RF almost inhibited the dramatic loss of glutathione peroxidasebased antioxidant scavenging efciency that was induced by MD, and in parallel strongly enhanced the gene expression of catalase-based antioxidant protection. In addition, RF abolished the MD-dependent down-regulation of oxoguanine DNA glycosylase, which is a critical DNA repairing enzyme. Overall, our fndings suggested that RF pre-exposure reduced menadione-dependent DNA oxidative damage, most probably by enhancing antioxidant scavenging efciency and restoring DNA repair capability. Our results provided some insights into the molecular mechanisms underlying the RF-induced adaptive response in human neuroblastoma cells challenged with menadione.
Protective effect of 1950 MHz electromagnetic feld in human neuroblastoma cells challenged with menadione
Anna Sannino;Stefania Romeo;Olga Zeni;
2018
Abstract
This study aims to assess whether a 1950 MHz radiofrequency (RF) electromagnetic feld could protect human neuroblastoma SH-SY5Y cells against a subsequent treatment with menadione, a chemical agent inducing DNA damage via reactive oxygen species formation. Cells were pre-exposed for 20h to specifc absorption rate of either 0.3 or 1.25W/kg, and 3h after the end of the exposure, they were treated with 10µM menadione (MD) for 1h. No diferences were observed between sham- and RFexposed samples. A statistically signifcant reduction in menadione-induced DNA damage was detected in cells pre-exposed to either 0.3 or 1.25W/kg (P<0.05). Moreover, our analyses of gene expression revealed that the pre-exposure to RF almost inhibited the dramatic loss of glutathione peroxidasebased antioxidant scavenging efciency that was induced by MD, and in parallel strongly enhanced the gene expression of catalase-based antioxidant protection. In addition, RF abolished the MD-dependent down-regulation of oxoguanine DNA glycosylase, which is a critical DNA repairing enzyme. Overall, our fndings suggested that RF pre-exposure reduced menadione-dependent DNA oxidative damage, most probably by enhancing antioxidant scavenging efciency and restoring DNA repair capability. Our results provided some insights into the molecular mechanisms underlying the RF-induced adaptive response in human neuroblastoma cells challenged with menadione.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.


