Cell phone exposure induces apoptosis, mitochondrial oxidative stress & TRPV1 channel activation in hippocampus of rats
Abstract
Overview
Recent advancements in mobile communications involve emission frequencies primarily at 900 and 1800 MHz, raising potential concerns on neuronal integrity.
Findings
- The study employed a rat model segregated into three groups: control, 900 MHz exposure, and 1800 MHz exposure.
- Significant increases in TRPV1 currents, Ca2+ influx, ROS production, mitochondrial depolarization (JC-1), and caspase activities were observed in neuronal samples from the hippocampus and dorsal root ganglion.
- Detrimental effects, including heightened apoptosis levels, were particularly escalated in the 1800 MHz group compared to the 900 MHz group.
Conclusion
The findings underscore a dose-related increase in mitochondrial oxidative stress and apoptosis associated with EMR exposure frequencies. TRPV1-mediated stress response is prominently implicated in this model, advocating for further research into the health impacts of long-term cellular phone usage.