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Electromagnetic radiation (EMR) and epilepsy are reported to mediate the regulation of apoptosis and oxidative stress through Ca influx. Results of recent reports indicated that EMR can increase temperature and oxidative stress of body cells, and TRPV1 channel is activated by noxious heat, oxidative stress, and capsaicin (CAP). We investigated the effects of mobile phone (900 MHz) EMR exposure on Ca influx, apoptosis, oxidative stress, and TRPV1 channel activations in the hippocampus of pentylenetetrazol (PTZ)-induced epileptic rats. Freshly isolated hippocampal neurons of twenty-one rats were used in study within three groups namely control, PTZ, and PTZ + EMR. The neurons in the three groups were stimulated by CAP. Epilepsy was induced by PTZ administration. The neurons in PTZ + EMR group were exposed to the 900 MHz EMR for 1 h. The apoptosis, mitochondrial membrane depolarization, intracellular reactive oxygen species (ROS), and caspase-3 and caspase-9 values were higher in PTZ and PTZ + EMR groups than in control. However, EMR did not add additional increase effects on the values in the hippocampal neurons. Intracellular-free Ca concentrations in fura-2 analyses were also higher in PTZ + CAP group than in control although their concentrations were decreased by TRPV1 channel blocker, capsazepine. However, there were no statistical changes on the Ca concentrations between epilepsy and EMR groups. In conclusion, apoptosis, mitochondrial, ROS, and Ca influx via TRPV1 channel were increased in the hippocampal neurons by epilepsy induction although the mobile phone did not change the values. The results indicated that TRPV1 channels in hippocampus may possibly be a novel target for effective target of epilepsy. [ABSTRACT FROM AUTHOR]

Many of toxic effects elicited by exposure to environmental stressors including electromagnetic radiation (EMR) are reported to be mediated the regulation of apoptosis and oxidative stress through Ca2+ influx. Changes in the apoptotic process induce in most of the neurodegenerative diseases including epilepsy. However, there is no report of cell phone exposure on Ca2+ influx, apoptosis and oxidative stress in epileptic rats through TRPV1 cation channels. Therefore, we tested the effects of cell phone frequency (900 MHz) exposure on Ca2+ influx, apoptosis, oxidative stress and TRPV1 channel activations in the hippocampus of pentylentetrazol (PTZ)-induced epileptic rats. Twenty-one rats were used in study within three groups namely control, PTZ and PTZ+EMR. Epilepsy was induced introperitoneal administrations of PTZ. After 1 hour, the hippocampal neurons were freshly isolated from the rats. The neurons in 900 MHz and PTZ+EMR groups were exposed to the 900 MHz EMR for one hour. The apoptosis levels, caspase-3 and -9 activities, mitochondrial depolarization rate and cytosolic reactive oxygen species (ROS) levels were higher in PTZ and PTZ+EMR groups than in control. Cytosolic free Ca2+ [Ca2+] i concentration was also higher in epilepsy+capsaicine group than in control although its concentration was decreased by TRPV1 channel blocker, capsazepine. There was no statistical significance on the values between PTZ and PTZ+EMR groups. In conclusion, in our experimental model, epilepsy but not cell phone-induced EMR (900 MHz) exposure induced Ca2+ influx (via TRPV1 channel activation), apoptosis and oxidative stress in the hippocampus neurons. We were not able to see risk on use of cell phone in the epileptic hippocampus. [ABSTRACT FROM AUTHOR]