Hazardous health effects resulting from exposure to radiofrequency electromagnetic radiation (RF-EMR) emitted from cell phones have been reported in the literature. However, the cellular and molecular targets of RF-EMR are still controversial. The aim of this study was to examine the oxidant/antioxidant status in saliva of cell phone users. Saliva samples collected before using a cell phone as well as at the end of 15 and 30 min calls were tested for two commonly used oxidative stress biomarkers: malondialdehyde (MDA) and 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-Oxo-dG). The 8-oxo-dG levels were determined by enzyme-linked immunosorbent (ELISA) competitive assay, while the MDA levels were measured using the OxiSelect MDA adduct ELISA Kit. The antioxidant capacity of the saliva was evaluated using the oxygen radical absorption capacity (ORAC) and the hydroxyl radical averting capacity (HORAC) assays according to the manufacture instructions. The mean 8-oxo-dG and the Bradford protein concentrations (ng/ml and mg/ml, respectively) peaked at 15 min. The levels of HORAC, ORAC and MDA progressively increased with time and reached maximum at 30 min. However, there was no significant effect of talking time on the levels of 8-OxodG and MDA. Similarly, there was no statistically significant effect of talking time on the oxygen and hydroxyl radicals averting capacities, (ORAC) and (HORAC), respectively. These findings suggest that there is no relationship between exposure to radio frequency radiation (RFR) and changes in the salivary oxidant/antioxidant profile.
We examined the effect of exposure to mobile phone 1800 MHz radio frequency radiation (RFR) upon the urinary excretion of 8-oxo-7, 8-dihydro-2'-deoxyguanosine (8-oxodG), one major form of oxidative DNA damage, in adult male Sprague-Dawley rats. Twenty-four rats were used in three independent experiments (RFR exposed and control, 12 rats, each). The animals were exposed to RFR for 2 h from Global System for Mobile Communications (GSM) signal generator with whole-body-specific absorption rate of 1.0 W/kg. Urine samples were collected from the rat while housed in a metabolic cage during the exposure period over a 4-h period at 0.5, 1.0, 2.0 and 4.0 h from the beginning of exposure. In the control group, the signal generator was left in the turn-off position. The creatinine-standardized concentrations of 8-oxodG were measured. With the exception of the urine collected in the last half an hour of exposure, significant elevations were noticed in the levels of 8-oxodG in urine samples from rats exposed to RFR when compared to control animals. Significant differences were seen overall across time points of urine collection with a maximum at 1 h after exposure, suggesting repair of the DNA lesions leading to 8-oxodG formation.
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