Calcium channel blockade alleviates brain injury induced by long term exposure to an electromagnetic field

This study aimed to examine the effects of short and long term exposures to 81 mG EMF intensity. It focused on the roles of ROS, Ca(2+) and calcium channel blocker (CCB) on the rat brain. Rats were exposed to 81 mG EMF intensity at the mobile phone base station for one and four weeks (2 hr/day, EMF exposed group). Another group of rats was pretreated with CCB (amlodipine 20 mg/kg) for four weeks and similarly exposed to EMF (EMF + amlodipine group). Sham exposed and amlodipine control groups were used. At the end of the study, Ca(2+) as well as pro-inflammatory and oxidative stress markers were measured. Immunohistochemical staining for Bax in brain samples was carried out. Short term exposure evoked a cellular adaptation response. This was evident by a transient increase in brain levels of Ca(2+), glutathione (GSH) and serum tumor necrosis factor alpha (TNF alpha). Long term exposure to EMF was lethal; progressive oxidative damage, and a prolonged increase in the Ca(2+) level accompanied by a marked pro-inflammatory reaction (TNF alpha and CRP) were demonstrated. These alterations were ameliorated by pre- and con-comitant treatment with amlodipine. Furthermore, it restored the EMF induced apoptosis in brain to near normal. In conclusion, EMF is a stressor agent that induces an imbalance between ROS generation and antioxidant defense response. Calcium ions may play a pivotal role in enhancing oxidative stress, pro-inflammatory reactions and apoptosis associated with EMF exposure. Therefore calcium channel blockade seems to play a role in brain protection.