This influence could be achieved through interaction of ELF-MF with chemical bonds between adjacent atoms leading to change in reaction between biomolecules and disruption of biomembrane changing structure of its protein molecules. Based, among others, on this mechanism, ELF-MF activates free radical species and prolongs their life. In our experiment, ELF-MF increased production of NO in all examined brain structures on the 7th exposure day with returning to control level 7 days after cessation of exposure. This increase is in line with previous findings. Activity of NO synthase is mediated through increase of intracellular Ca2+, event that occurs as a consequence of the applied ELF-MF. In case when we exposed ischemic gerbils to ELF-MF, NO content was slightly lower then in only ischemic gerbils on the 7th day after reperfusion, and at the control level on the 14th day after reperfusion. Having in mind that cerebral ischemia also increases influx of Ca2+, someone could WZ8040 expect that the effect of ELFMF would be cumulative leading to additional increase of NO content. The same results are observed with ILP meaning that ELF-MF could attenuate harmful effects of ischemia on membranes and reduce further ROS and RNS production. Like in our case, in the majority of experiments ELF-MF increases lipid peroxidation. We can propose that ELF-MF, through increasing the level of NO, is involved in the reduction of ILP in ischemic gerbils, because NO itself may directly inhibit lipid peroxidation by intercepting alkoxyl and peroxyl radical intermediates and thus terminating chain propagation reaction. Di Loreto et al. also proposed that ELF-MF can simultaneously activate proand antioxidants. They applied ELF-MF on cortical neurons and beside increased production of ROS and malondialdehyde, they also found increased expression of brain-derived neurotrophic factor and nerve growth factor, proteins which participate in free radical clearance. ELF-MF per se increased O2 2 content on the 7th exposure day, but when applied in ischemic gerbils it reduced production of this free radical species. Important finding is that the activity of SOD, enzyme which dismutases O2 2, was not increased in ischemic gerbils, but it was increased in ELF-MF exposed gerbils without or with induced global cerebral ischemia on the 7th exposure day. Our findings are in accordance with some papers, but also there are some opposite results. This means that ELF-MF activates one of the most important enzyme of antioxidant defense and through reduction of O2 2 level decreases further propagation of oxidative stress event. The most interesting result of this study is that ELF-MF and ischemia separately increase oxidative stress, but when applied together they have capability to decrease values of measured parameters.