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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]