Protective effect of radiofrequency exposure against menadione‐induced oxidative DNA damage in human neuroblastoma cells: The role of exposure duration and investigation on key molecular targets

In our previous studies, we demonstrated that 20 h pre‐exposure of SH‐SY5Y human neuroblastoma cells to 1950 MHz, UMTS signal, at specific absorption rate of 0.3 and 1.25 W/kg, was able to reduce the oxidative DNA damage induced by a subsequent treatment with menadione in the alkaline comet assay while not inducing genotoxicity per se. In this study, the same cell model was used to test the same experimental conditions by setting different radiofrequency exposure duration and timing along the 72 h culture period. The results obtained in at least three independent experiments indicate that shorter exposure durations than 20 h, that is, 10, 3, and 1 h per day for 3 days, were still capable to exert the protective effect while not inducing DNA damage per se. In addition, to provide some hints into the mechanisms underpinning the observed phenomenon, thioredoxin‐1, heat shock transcription factor 1, heat shock protein 70, and poly [ADP‐ribose] polymerase 1, as key molecular players involved in the cellular stress response, were tested following 3 h of radiofrequency exposure in western blot and qRT‐PCR experiments. No effect resulted from molecular analysis under the experimental conditions adopted. Highlights RF exposure of human neuroblastoma cells at 1950 MHz, UMTS signal, does not induce genotoxicity per se at 0.3 and 1.25 W/kg SAR. RF exposure reduces the MD‐induced genotoxicity in several time windows along the 72 h cell culture period at both SAR levels. RF exposure does not alter protein and gene expression of key molecular players involved in cellular stress response in the assay conditions adopted.