Abstract. Oxidative stress may affect many cellular and physiological processes including gene expression, cell growth, and cell death. In the recent study, we aimed to investigate whether 900 MHz pulse-modulated radiofrequency (RF) fields induce oxidative damage on lung, heart and liver tissues. We assessed oxidative damage by investigating lipid peroxidation (malondialdehyde, MDA), nitric oxide (NO x ) and glutathione (GSH) levels which are the indicators of tissue toxicity. A total of 30 male Wistar albino rats were used in this study. Rats were divided randomly into three groups; control group (n = 10), sham group (device off, n = 10) and 900 MHz pulsed-modulated RF radiation group (n = 10). The RF rats were exposed to 900 MHz pulsed modulated RF radiation at a specific absorption rate (SAR) level of 1.20 W/kg 20 min/day for three weeks. MDA and NO x levels were increased significantly in liver, lung, testis and heart tissues of the exposed group compared to sham and control groups (p < 0.05). Conversely GSH levels were significantly lower in exposed rat tissues (p < 0.05). No significantly difference was observed between sham and control groups. Results of our study showed that pulse-modulated RF radiation causes oxidative injury in liver, lung, testis and heart tissues mediated by lipid peroxidation, increased level of NO x and suppression of antioxidant defense mechanism.

The overall findings indicated that whole body exposure to pulse-modulated RF radiation that is similar to that emitted by global system for mobile communications (GSM) mobile phones can cause pathological changes in the thyroid gland by altering the gland structure and enhancing caspase-dependent pathways of apoptosis.

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Electrochemotherapy is the usage of electroporation to introduce chemotherapeutic drugs through membrane pores into target cells for cancer treatment. The effectiveness of chemotherapeutic drugs would be increased dramatically when they are used in electrochemotherapy than standard chemotherapy. In the present study, we investigated the effects of cisplatin treatment with electroporation on human SH-SY5Y neuroblastoma cells. SH-SY5Y cells were treated with different concentrations (0.15-24 µg/mL) of cisplatin and then exposed to 1500 volts per centimeter (V/cm), 100 microseconds (µs) pulse duration, and 1 Hertz (Hz) electric pulses. Cisplatin alone showed a dose-dependent effect on cell viability. On the other hand, cisplatin + electroporation treatment was more effective than cisplatin treatment alone. Lower doses of cisplatin treatment with electroporation was as effective as higher doses of cisplatin treatment without electroporation. These results indicated that cisplatin cytotoxicity was potentiated after exposure of cells to high intensity electric pulses and low doses of cisplatin can be used with electroporation in the treatment of neuroblastoma.

This study examines the effects of a 2.1-GHz WCDMA-modulated microwave (MW) radiation on apoptotic activity and mitochondrial membrane potential (ΔΨm) in MCF-7 cells. The cells were exposed to the MW at a specific absorption rate (SAR) of 0.528 W/kg for 4 or 24 h. The antiproliferative effect of MW exposure was determined by the MTT test. Cytochrome-c and p53 levels were determined by an ELISA method. The relative ΔΨm was analysed by JC-1 staining using flow cytometer. Apoptotic rate of the cells was measured by Annexin-V-FITC staining. All assays were performed after certain time of incubations (15 min-4 h) following MW exposure. MW-exposed cells showed a significant decrease in viability when compared to unexposed cells. A significantly larger decrease was observed after longer exposure. The percentage of apoptotic cells, amount of cytochrome-c, and relative ΔΨm were significantly higher in MW-exposed cells. The percent of apoptotic cells and relative ΔΨm in 24 h MW-exposed group was significantly higher than those in 4 h MW-exposed group. However, no significant change was observed in p53 levels. These results demonstrated that exposure to 2.1-GHz WCDMA-modulated MW radiation caused hyperpolarization of mitochondria that in turn induced apoptosis in MCF-7 cells.

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