306 Discussion Se is important for the control of oxidative stress and therefore the redox state of the cell, due to its incorporation as selenocysteine to GSH-Px [19] and thioredoxin reductase [20]. Selenium, as an essential micronutrient in animals, has three levels of biological activities: (1) trace levels are required for normal growth and development, (2) nutritional and supra- nutritional levels can be stored, and homeostatic functions will be maintained, and (3) toxic levels can result in harmful effects [21]. TBARS in biological specimens, including lipid hydroperoxides and aldehydes, increase as a result of oxidative stress. Indeed, plasma concentrations of TBARS are an index of lipid perox- idation and oxidative stress. TBARS return to normal levels over time, depending upon the antioxidants [22, 23]. In this study, the TBARS value in group 1 (nano- selenium) was reduced after the 20th day, but in group 2 (sodium selenite), the TBARS value was in a high level till the 30th day. Therefore, in group 2, the return of TBARS to the basal level has been done with more delay, and it shows the better antioxidative activity of selenium nanoparticles in comparison with sodium selenite. Kumar et al. indicated that Se had no effect on serum total protein, albumin/globulin ratio, and SGPT and SGOT activities but could increase the capacity of the immune system to protect cells from free radical injuries [24]. Huang et al. showed that the elemental Se nanoparticles have significant effects on both the scavenging of the free radicals and the protection of DNA against oxidation, dependent upon size: the smaller, the better [25]. The major result of increasing phagocytic activities of polynuclear cells, especially neutrophils, which are the first body defensive barriers, is an increase in oxidative pressure [26]. Also, respiratory burst, which occurred in neutrophils, can release oxygen free radicals that play a major role in pathogenesis of foreign agents. When neutrophils inter- act with foreign agents, hundreds of times more oxygen may be released than in their resting state. This causes increasing activation of the NADPH oxidase enzyme on the cell surface. Toxic materials that are produced in neutrophils are severely destructive and cause neutrophil membrane destruction. Selenium admixtures can prevent destruction by elimination of toxic materials and free radicals and can reduce toxic material production of neutrophils, lipid peroxidation, and TBARS values [27–29]. Zhang et al. indicated that nano-Se had a weaker interference effect than selenite on antioxidative balance in Se-deficient mice [13]. Selenium, as the functional component of GSH-Px, protects the neutrophils and other blood components against peroxidative damage [27]. Fraga has mentioned Sadeghian et al. that selenium deficiency can increase oxygen free radicals in body tissues [28], the major negative effects of which are on the consistency of biological membranes and the performance of immunity cells [30]. Heyland has suggested selenium meal consumption as a protective antioxidative activity and a way of decreasing acute disease mortality [31]. Selenium is involved in selenoprotein-type structures which include glutathione peroxidase [32], P selenoprotein, and W selenoprotein. These proteins have a protective role against oxidant materials in body cells and cause an increase in the body's cell resistance such as immunity cells against oxidative destruction [33, 34]. In a study, Zhou et al. indicated discrepancy of muscle Se concentration and GSH-Px activity is because only a part of nano-Se was adopted for selenoprotein synthesis and another metabolic pathway of nano-Se differing from sodium selenite and selenomethionine may exist [35]. The most important action Se is its antioxidant effects because it forms selenocysteine, part of the active center of the GPx [36, 37]. GPx is the most important peroxidase for the detoxification of hydroperox- ides and lipidic hydroperoxides at the level of the cytosol and mitochondrial matrix [38, 39]. Nano-Se increased the GST activity more efficiently than selenomethionine [11]. The higher antioxidative activity of nano-Se is further evident from the observed decline of the hepatic superoxide dismutase (SOD) activity. Furthermore, nano-Se exhibits stronger inhibitory effects than selenite and simultaneously increases the hepatic GSH (reduced glutathione) concen- trations, while no apparent alteration of the GSH levels were observed with selenite [40]. Since SOD and GSH are indicators of oxidative stress, this demonstrates the advan- tages of nano-Se over other forms of the element. What should be noted about the changes in hematological parameters is the effect of selenium on survivability of the RBCs [41]. Fraga and Lessard have recognized selenium deficiency as a factor in preventing the activity of glutathione peroxidase and increasing the free oxygen radicals in the tissues such as RBCs, which leads to increase the oxidative damage of the tissues [28, 30]. Although the role of selenium in increasing the resistance of the RBCs has been proved and its deficiency has been mentioned as a factor in anemia production, this effect has not been significant when studying the hematological profile in the present study, and the number of RBCs and the hematocrit value in the group getting nano-selenium have been a little more than group 2 (sodium selenite) and the control group, but not statistically significant. It should be mentioned about the changes in the number of neutrophils, lymphocytes, and WBCs, that the type of body immunity system response and the leukogram changes would be different depending on the kind of animal, individual differences, the kind of animal's nutrition, the grade of the animal's involvement, the