The Reactive Oxygen Species (ROS) and the Reactive Nitrogen Species (RNS) are highly reactive molecules participating as mediators in biological processes such as metabolic cellular respiration, neurotransmission, translation and transcription gene, and inflammatory-type reactions among others (D. Almaguer & L.E. Almaguer, 2006; Boots et al., 2008; Uttara, 2009). Additionally, these molecules have the capacity to interact with nucleophilic centers of biomolecules by modulating their activity or by irreversibly modifying them in order to generate different kind of radicals (D. Almaguer & L.E. Almaguer, 2006). The main oxygen radicals are the hydroxyl (-OH), the superoxide anion (O2-), and the hydrogen peroxide (H2O2), while the main nitrogen radical is the nitric oxide (•NO), but also, it is known that the ROS can interact with -NO generating new species with high oxidizing power (Martinez et al., 2010). In aerobic systems most of the ROS come from the mitochondrial oxidative metabolism, where 1-2% of the oxygen is converted into free radicals (Uttara et al., 2009). Other less important sources of ROS are the autoxidation of catecholamines and hemoproteins that occurs in the cytoplasm, nuclear membrane, endoplasmic reticulum and peroxisomes (Boots et al., 2008; Martinez et al, 2010). The concentration of ROS or RNS in organisms is determined by the balance between the rate of production of reactive species and the elimination rate of these compounds by the action of enzymes and antioxidants (AO) (Dorado et al., 2003). Thus, under conditions of physiological homeostasis, a balance exists between the cellular processes that contribute to the production of ROS / RNS, and those factors such as superoxide dismutase (SOD), catalase (Cat) and glutathione peroxidase (GPx), which contribute to their elimination (Dorado et al., 2003; Martinez et al., 2010). Thus, alterations in the balance between these systems, pro-oxidants and antioxidants can lead to intracellular accumulation of free radicals (FR), causing oxidative stress states (Dorado et al., 2003; Kelsey, et al , 2010; Uttara, 2009). Specifically, oxidative stress and redox imbalance is the combined result of excessive formation of oxidant species (ROS/RNS) and/or a decreasing in the efficiency of endogenous antioxidant systems. Thus, the combination of these factors converge in damaging to biomolecules such as DNA, RNA, proteins, carbohydrates and lipids. This probably initiate processes of mitochondrial dysfunction and excitotoxicity (Kelsey, et al.,