High levels of ROS generation resulting from nicotinamide adenine dinucleotide phosphate oxidase, particularly associated with the activation of the innate immune system within the CNS. In both circumstances, oxidative stress results when imbalance between ROS production and the clearance of chemically reactive species by endogenous antioxidant enzymes and reducing agents occurs. Environmental factors such as ELF-EMFs, stressors, or disease that augment the former or lower the latter can amplify and drive the process. Thus, in practical terms, oxidative stress is determined by excessive exposure to oxidant molecules when there is insufficient availability of antioxidant mechanisms, with the resulting ROS oxidizing vulnerable cellular constituents, including proteins, nucleic acids and lipids, inducing microglial activation, inducing pro-inflammatory and suppressing anti-inflammatory cytokines and related signaling pathways, and ultimately CUDC-907 causing both synaptic and neuronal damage and dysfunction. In this regard, the neuronal properties of SH-SY5Y human neuroblastoma cells, together with their pronounced sensitivity to oxidative stress and inflammation, make these cells a valuable model to study a number of neurological pathologies at the molecular, morphological and physiological level. Previous studies have demonstrated that the cellular effects of ELF-EMFs depend, in large part, on their intensity and exposure time, as well as on the phenotype of the cellular target and interactions with intracellular structures. In SH-SY5Y cell cultures and a number of other cell types exposed to ELF-EMF, genes involved in the stress response, cell growth and differentiation or protein metabolism have been reported to be generally down-regulated, whereas genes involved in Ca2+ metabolism, the PI3-kinase pathway, trascription and it’s modulation by splicing are up-regulated. Such actions are reported to often be accompanied by changes in cell growth and oxidative balance. In our experimental conditions, timed continuous ELF-EMF ), 50 Hz) exposure likewise impacted cellular oxidative status, causing an early rise in NOS activity and O22 levels in SH-SY5Y cells. Within a short duration, this was counteracted by a compensatory increase in the antioxidant capacity of CAT to, thereby, provide the potential to more effectively scavenge any prospective ELF-EMF-mediated ROS over-production; thus avoiding oxidative ELF-EMF-induced cellular damage. In this regard, NOS activity peaked following 1 hr of ELF-EMF exposure and, thereafter, its level declined and remained approximately constant. Accompanying this, a rise in CAT activity was observed after 6 hr of ELF-EMF exposure that was associated with enzyme kinetic changes. In light of this, ELF-EMF exposure time-dependently elevated the rate of cellular O22 production, which peaked at 6 hr and, thereafter, declined toward the baseline value. Hence ELF-EMF exposure can be considered to induce an “activated” cellular state, wherein the enhanced generation and the release of free radicals is offset by a compensatory modulation of antioxidant defences, leading to an absence of negative effects on cell growth and viability.