부산대학교 도서관

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, Ca2+ 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, Ca2+ 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 Ca2+, glutathione (GSH) and serum tumor necrosis factor alpha (TNFα). Long term exposure to EMF was lethal; progressive oxidative damage, and a prolonged increase in the Ca2+ level accompanied by a marked pro-inflammatory reaction (TNFα 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. [ABSTRACT FROM AUTHOR]