Long term exposure to cell phone frequencies (900 and 1800MHz) induces apoptosis, mitochondrial oxidative stress and TRPV1 channel activation in the hippocampus and dorsal root ganglion of rats.

Abstract

Mobile phone providers use electromagnetic radiation (EMR) with frequencies ranging from 900 to 1800MHz. The increasing use of mobile phones has been accompanied by several potentially pathological consequences, such as neurological diseases related to hippocampal (HIPPON) and dorsal root ganglion neuron (DRGN). The TRPV1 channel is activated different stimuli, including CapN, high temperature and oxidative stress. We investigated the contribution TRPV1 to mitochondrial oxidative stress and apoptosis in HIPPON and DRGN following long term exposure to 900 and 1800MHz in a rat model. Twenty-four adult rats were equally divided into the following groups: (1) control, (2) 900MHz, and (3) 1800MHz exposure. Each experimental group was exposed to EMR for 60min/ 5days of the week during the one year. The 900 and 1800MHz EMR exposure induced increases in TRPV1 currents, intracellular free calcium influx (Ca2+), reactive oxygen species (ROS) production, mitochondrial membrane depolarization (JC-1), apoptosis, and caspase 3 and 9 activities in the HIPPON and DRGN. These deleterious processes were further increased in the 1800MHz experimental group compared to the 900MHz exposure group. In conclusion, mitochondrial oxidative stress, programmed cell death and Ca2+ entry pathway through TRPV1 activation in the HIPPON and DRGN of rats were increased in the rat model following exposure to 900 and 1800MHz cell frequencies. Our results suggest that exposure to 900 and 1800MHz EMR may induce a dose-associated, TRPV1-mediated stress response.