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Nutritional modulation of the antioxidant capacities in poultry.
Natural antioxidants play important roles in maintaining chicken health, productive and reproductive performance of breeders, layers, rearing birds and growing broilers. There is a wide range of antioxidant molecules in the body: vitamin E, carotenoids, selenium, ascorbic acid, coenzyme Q, carnitine, taurine, antioxidant enzymes, etc. In the body all antioxidants work together to create the antioxidant network called “antioxidant systems” with Se being the “chief-executive”. Analysis of the current data on selenium roles in antioxidant defences in poultry clearly showed its modulatory effect at the level of breeders, developing embryos, newly hatched chicks and postnatal chickens. From the one hand, Se is involved in expression and synthesis of 26 selenoproteins, including GSH-Px, TrxR and SepP. On the other hand, Se affects non-enzymatic (vitamin E, CoQ and GSH) and enzymatic (SOD) antioxidant defence mechanisms helping build strong antioxidant defences. Se efficiency depends on the level of supplementation and form of dietary Se, organic Se sources being more effective modulators of the antioxidant systems in poultry than sodium selenite. Moreover Se levels in eggs from some wild avian species are close to those found in chicken eggs after 0.3 ppm organic Se supplementation and a search for most effective dietary form of organic Se is a priority in poultry nutrition. It seems likely that antioxidant/prooxidant (redox) balance of the gut and the role/interactions of Se and microbiota in maintaining gut health would be a priority for future poultry research.
Natural antioxidants play important roles in maintaining chicken health, productive and reproductive performance of breeders, layers, rearing birds and growing broilers. There is a wide range of antioxidant molecules in the body. Some of them are supplied with feed (vitamin E, carotenoids, selenium), others are synthesised in tissues (ascorbic acid, coenzyme Q, carnitine, taurine, antioxidant enzymes, etc.). In the body all antioxidants work together to create the antioxidant network called “antioxidant systems” (Surai, 2002; 2006; 2016; 2017). In this network all antioxidants are closely connected to each other via various mechanisms, including stress-response elements, transcription factors (Nrf2, NF-kB, etc.), vitagenes and other important elements (Surai, 2016; Surai and Fisinin, 2016c). In recent years, redox balance of the cell and reactive oxygen species (ROS) signaling have received tremendous attention and understanding of the antioxidant defence strategy in the cell/body is among important priorities in biochemistry and cell biology. Taking into account stressful conditions of commercial poultry production, regulation of the antioxidant defence systems of poultry by nutritional means become a topic of great interest. Indeed, by inclusion into the poultry diet of optimal levels of vitamin E, selenium, carotenoids in combination with other compounds possessing antioxidant properties (carnitine, taurine, etc.) it is possible to provide a maximum protection in stress condition and maintain productive and reproductive performance of poultry at the highest level. In this review an analysis of data on the effect of Se on the antioxidant defence network in poultry is presented.
Stresses in poultry production and free radical production
Commercial poultry production is associated with a range of stresses. They can be divided into 4 main categories, including environmental (deviation from optimal temperature, increased ammonia or dust, excessive noise, etc.), technological (chicken placement, grading, debeaking, vaccinations, etc.), nutritional (mycotoxins and oxidised fat, imbalance of nutrients, etc.) and biological/internal (hatching, high growth rate, disease challenge, etc.) stresses (Surai and Fisinin, 2016; 2016a). For the last four decades information has been actively accumulated to suggest that most stresses at the molecular level are associated with overproduction of free radicals and oxidative stress (Surai, 2002; 2006; 2016). In fact, it has been shown that electron transport chain of mitochondria is the main source of free radicals in biological systems. Indeed, up to 3% of oxygen can escape from the energy production process and become free radicals which can damage all types of biological molecules including lipids, proteins and DNA. Furthermore, phagocyte cells are considered to be the second most important source of free radicals in the body. In this case free radical production is absolutely an essential process and these reactive molecules are used as a weapon to kill pathogens. However, once these radicals escaped phagosome they can damage healthy tissues (Surai, 2006). There are also other processes in the body, including xenobiotic metabolism and detoxification, prostanoids synthesis, inflammatory responses, etc., producing free radicals. Furthermore, there is a range of internal and external factors increasing free radical production, including presence of transition metals (Fe2+ and Cu+), high levels of PUFAs, high oxygen concentration, etc. (Surai, 2002;2006).
To deal with various types of free radicals during evolution protective defence mechanisms called antioxidant systems have been developed, shaped and they are responsible for survival higher eukaryotes in oxygenated atmosphere. They include fat-soluble (vitamin E, carotenoids and coenzyme Q; CoQ), water-soluble (ascorbic acid, glutathione, thioredoxin, carnitine, taurine, etc.) antioxidants and antioxidant enzymes (superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and other selenoproteins, catalase, glutathione reductase, glutathione transferase, etc.). In many cases synthesis of internal antioxidants, including SOD, selenoproteins and CoQ in response to stress conditions is an adaptive mechanism to prevent negative consequences of stresses. In fact, a redox balance of the cell/tissue/body is responsible for adaptive regulation of the antioxidant defences and transcription factors such as Nrf2 and NF-kB are involved in this process. Indeed, recently free radicals have been considered to be signaling molecules regulating adaptation to stress (Reczek and Chandel, 2015). Furthermore, from 26 selenoproteins in avian species more than half directly or indirectly involved in the antioxidant defence network and/or in maintenance of redox state of the cell. In particular, four known Se-dependent GSH-Px in poultry are involved in all three levels of antioxidant defence (Surai, 2006). Recently a vitagene concept has been developed and successfully applied to poultry production (Surai and Fisinin, 2016b; 2016c). In accordance with this concept there is a range of genes encoding for protective molecules such as SOD, thioredoxin system, HSP, sirtuins, etc. which regulate adaptive ability of the cell/tissue/body to various stress conditions.
Choice of a model system to address antioxidant system modulation
To address the nutritional modulation of antioxidant defences in poultry, a chain, including breeder-egg-newly hatched chick-posthatch chick was chosen as a model system. First of all, there is an opportunity to observe antioxidant effects at all the stages of this model. Secondly, egg yolk (Speake et al., 1998) and chick embryonic tissues (Surai et al., 1996) are rich in polyunsaturated fatty acids making them to be very sensitive to oxidative stress and need for effective antioxidant protection. Thirdly, transfer of antioxidants to the newly hatched chick and their protection from various stresses in early postnatal life is key for the development of vital functions in poultry including immune and digestive system (Surai and Fisinin, 2015). Finally effect of antioxidants in the maternal diet on the antioxidant defences in growing chicks could show possible epigenetic effects (Surai, 2002; 2006).
The antioxidant system of the chicken embryo and newly hatched chick includes the fat-soluble antioxidants vitamin E, carotenoids, and coenzyme Q (CoQ,), water-soluble antioxidants ascorbic acid, glutathione , carnitine, taurine (Surai, 2002; 2017) as well as antioxidant enzymes superoxide dismutase (SOD), GSH-Px, catalase (Surai, 2016), TR (Xiao et al., 2016) and selenium as a part of various selenoproteins (Surai, 2006; Pappas et al., 2008; Surai and Fisinin, 2016d). Vitamin E and carotenoids are transferred from feed into egg yolk and further to embryonic tissues. Similarly, Se is transferred from the feed to the egg yolk and albumin (Surai and Fisinin, 2014) and further to the developing embryo (Surai, 2006; Surai and Fisinin, 2016d).
From a range of antioxidants provided by the feed ingredients and feed supplements, only selenium (as a precursor of selenoprotein synthesis), vitamin E and carotenoids can be used in this model. Dietary manipulation of the aforementioned nutrients is used for many years to improve antioxidant defences in commercially-relevant stress conditions of the industrial poultry production.
Roles of Se in antioxidant defence network modulation
Trace element selenium (Se) was discovered 200 years ago, its essentiality in animal and human nutrition was proven in 1957 and first selenoprotein called GSH-Px was described in 1973 (Surai, 2006). Recently a family of chicken selenoproteins has been updated to include 26 genes responsible for selenoprotein synthesis (Lei, 2017; Zhao et al., 2017). Indeed, it is proven that selenium in the form of SeCys performs its functions as an essential part of various selenoproteins which are important elements/modulators of the antioxidant network in poultry/animal body.
Selenium requirement and availability
In feed ingredients including wheat, barley, corn and soya Se is found mainly in organic form, with SeMet representing more than 50% of total Se. However, Se concentration in feed is very variable and in most parts of the world is quite low. Therefore, to deal with a global Se deficiency, poultry and farm animal diets started to be supplemented with Se in 1970th (Surai, 2006). The Se requirements of poultry have been shown to be quite low, ranging from 0.06 mg/kg diet for laying hens (Surai and Fisinin, 2014) up to 0.2 in broiler chicks (Li and Sunde, 2016) and 0.3 mg/kg diet for turkeys (Taylor and Sunde, 2016). However, in stress conditions Se requirement could be substantially increased and nowadays Se is incorporated in major premixes for all categories of poultry at 0.1-0.3 ppm in various forms including sodium selenite, selenate and organic forms of selenium namely Se-Yeast, SeMet, OH-SeMet, Zn-SeMet (Surai, 2006; Surai and Fisinin, 2014; 2016d). In layers Se availability from a basal diet containing 0.18 mg Se/kg was indicated to be 85.5%, while in the same diet supplemented with 0.3 ppm sodium selenite or Se-yeast the Se bioavailability is shown to be 51.6 and 67,2% respectively (Chantiratikul et al., 2017). The main task for poultry nutritionist is to provide an optimal Se status of the breeders for maintenance of their health, productive and reproductive performance. Since selenoprotein synthesis is genetically and environmentally regulated, only an optimal dietary supplementation will provide maximal Se-protein expression. The most important feature of Se metabolism and Se-protein synthesis is a fact that Se- proteins are synthesized as needed for their functions. In fact there are two fundamental factors regulating Se-protein expression and syntheses namely Se status and level of stress reflected by the redox balance of the cell (Gladyshev, 2016).
Modulating effects of dietary Se
Main advantage of Se for breeders is related to building Se reserves in the body which can be used in stress conditions when Se requirement increases but very often feed consumption decreases (Surai, 2006). This reserve can be built in muscles only with dietary SeMet which is non-specifically incorporated into proteins in place of methionine. In stress conditions protein catabolism and activation of proteasome will release Se providing it for additional synthesis of selenoproteins and improved antioxidant defences (Surai and Fisinin, 2016). In fact, it was shown that the intracellular redox status, is an important element activating or down-regulating the 20S proteasome chymotrypsin-like activity in living cells (Kretz-Remy and Arrigo, 2003). This is a very important finding, which explains how Se-reserves in the body can be used to improve antioxidant defences in stress conditions. Indeed, dietary supplementation of organic Se (0.4 mg/kg) to quail was associated with elevated Se concentration in their breast muscles from 0.13 (non-supplemented diet) up to 0.44 mg/kg (Surai et al., 2006) therefore increasing the Se reserves more than 3 times. Similarly, inclusion of organic Se into the diet is associated with a significant increase Se level in breeder muscles. For example, when SS or Se-Yeast were included into the diet at 0.3 ppm, Se concentration in breast muscle (ppm) in non-supplemented birds, SS and Se-Yeast-supplemented breeders were 0.42; 0.39 and 1.22 showing almost 3-fold increase due to organic Se supplementation (Invernizzi et al., 2013). Similarly in laying hens fed on the basal diet or the same diet supplemented with 0.3 mg Se/kg as SS, Se-Yeast or SeMet, Se concentrations in the breast muscle were (mg/kg) 0.64; 0.69; 1.01 and 1.42 respectively (Jing et al., 2015). Again SeMet supplementation of the layer diet was associated with more than doubled Se reserves in the breast muscle. These data clearly showed that organic Se in the breeder diet could directly (by activating GSH-PX) or indirectly (by increasing vitamin E levels) improve antioxidant defences of birds. In the same study Jing et al. (2015) showed a significant increase in GSH-Px and SOD activity in their plasma due to dietary Se supplementation. In the study Se-Yeast and SeMet upregulated GSH-Px more effectively than SS. Furthermore, adding sodium selenite at 0.5 ppm into the diet of breeding pigeon was associated with increased GSH-Px activity in plasma, liver, breast and leg muscles and SOD activity in plasma and decreased lipid peroxidation in plasmas in comparison to non-supplemented control birds (Wang et al., 2017). In addition, there was an increased expression of GSH-Px4 in testis and ovary due to Se supplementation. When gene expression was studied in the oviduct of Se-supplemented (0.3 ppm) breeders, it was shown that there was a significant difference between different forms of Se. In fact Se-Yeast, but not SS, increased transcripts of GPX4 and SEPP1. They were significantly upregulated (1.78- and 1.81-fold, respectively) in Se-Yeast-fed hens but remained unaffected in SS birds (Wang et al., 2017).
Furthermore, Se-Yeast was shown to up-regulate multiple genes involved in oxidative phosphorylation, mitochondrial function and ubiquinone biosynthesis (Brennan et al., 2011). At the same time SS was shown to downregulate genes involved in oxidative phosphorylation and did not affect gens involved in ubiquinone synthesis. It should be mentioned that ubiquinone is an important fat-soluble antioxidant and electron carrier synthesized in mitochondria (Stefely and Pagliarini, 2017). It directly involves in protection of lipids, proteins and DNA from oxidative damage by quenching free radicals, regenerating other antioxidants (vitamins E and C) and regulating mitochondrial integrity (Varela-López et al., 2016). It was suggested that Se inadequacy could compromise the cells ability to obtain the optimal concentrations of coenzyme Q10, while optimal function of Se depends on the levels of coenzyme Q10 (Alehagen and Aaseth, 2015). It seems likely that, additional synthesis of CoQ in stress conditions is an adaptive mechanism to deal with overproduction of free radicals. Indeed, oxidative stress is associated with increased coenzyme Q synthesis reflecting cellular adaptation. For example, 18 hour holding chicks in the incubator posthatch was associated with a significant increase CoQ levels in the liver (Karadas et al., 2011). Furthermore, increased CoQ concentration was observed in vitamin E and Se deficient rats (Navarro et al., 1998). In general, increased expression of CoQ due to Se supplementation is a great contribution to the antioxidant network efficiency.
In the experiment conducted in China (Yuan et al., 2012) broiler breeders were fed corn-soy-based diets supplemented with 0.15 mg/kg of Se from SS, Se-Yeast or SeMet. The results showed that, compared with SS, Se-Yeast or SeMet significantly increased the activity of TrxR1 in the liver and kidney and expression of GSH-Px in the liver of broiler breeder birds. Interestingly, TrxR enzymes are essential components of the thioredoxin system consisting of thioredoxin, thioredoxin peroxidases (peroxiredoxins) and thioredoxin reductase. This system plays a vital role in regulating multiple cellular redox signaling pathways, including the antioxidant defence network, regulation of gene transcription and expression, DNA synthesis and repair, protein biosynthesis, hormone and cytokine action, apoptosis, etc. (Lu and Holmgren, 2014). According to Smith et al. (2001) and Gowdy (2004) in comparison with mammals, chickens have extremely low TrxR activities. Recently, TrxR activity has been determined in various chicken tissues including liver, lung, heart, kidney, brain, breast muscle, bursa, thymus, spleen, RBC and plasma (Gowdy et al., 2015). It is proven that activity of chicken TrxR is selenium dependent. Subcellular distribution of TrxR activity was found in association with cytosolic, nuclear pellet and mitochondrial fractions. Selenium dietary supplementation (0.4 mg/kg diet) increased TrxR activity in duodenal mucosa, liver and in the kidney in chickens (Placha et al., 2014). Se deficiency was associated with a decreased expression of TrxR2 in chicken thyroids (Lin et al., 2014). Similarly, Se deficiency in chickens was associated with a significant decrease in activity of TrxR1 (by 50%), TrxR2 (by 83%) and TrxR3 (by 36%) in the pancreas (Zhao et al., 2014). Furthermore, TrxR activity decreased in chicken adipose tissues due to Se deficiency (Liang et al., 2014). A low Se diet (0.028 mg.kg) or high Se diet (3 mg/kg) significantly reduced the TrxR activity in chicken kidney, with changes observed in mRNA levels. In particular, the low Se diet downregulated the mRNA expression of TrxR3 (Xu et al., 2016). Recently, it has been proposed that TrxR1 is a potent regulator of Nrf2 playing a central role in redox homeostasis, defense against oxidative stress, and regulation of redox signaling pathways (Cebula et al., 2015).
It has been shown that organic Se (Se-Yeast or SeMet) supplementation of the breeder diet (0.15 mg/kg) was associated with increased concentration of SepP1 in the serum and liver and enhanced SepP1 expression in the liver in comparison to birds receiving sodium selenite (Yuan et al., 2013). Interestingly, SepP is the major plasma selenoprotein, which is synthesized primarily in the liver and delivers Se to certain other organs and tissues (Gladyshev, 2016; Schweizer et al., 2016). Furthermore, it has been suggested that SepP might have an important role as an antioxidant in plasma (Steinbrenner et al., 2006) acting as an extracellular PH-GSH-Px (Saito et al., 1999). Importantly, selenoprotein (e.g. GSH-Px) response to dietary Se depends on many factors and in the case of adequate Se in the diet additional Se supplementation would not increase activity of the enzyme. For example in a recent study of Delezie et al., (2014) background Se level was 0.25 mg/kg and adding additional Se at 0.1, 0.3 or 0.5 mg/kg in different forms did not affect GSH-Px activity in serum of experimental birds.
The second part of the evidence proving antioxidant modulating properties of Se are related to the effect of maternal Se on the egg, developing embryo, newly hatched chick and chicken in early postnatal life. The supplementation of the diet with Se is an effective way to increase Se concentrations in whole egg (for review see Surai and Fisinin, 2014). Recently it has been determined that SeMet comprised 53–71% of total Se in the egg albumen and 12–19% in the egg yolk (Lipiec et al., 2010). Therefore, SeMet can be non-specifically incorporated into the egg proteins in place of methionine and its level would depend on the ratio SeMet/Met in the feed. It was calculated that in the basic starter chicken diet the ratio of SeMet:Met is about 1:60,000; in the growing diet it is 1:50,000 and this ratio is almost the same for breeder birds (Schrauzer and Surai, 2009; Surai and Fisinin, 2014). This ratio can be changed to 1: 12-15,000 after dietary Se supplementation in the form of SeMet at 0.3 mg/kg. The calculation also showed that the ratio of SeMet/Met in the egg yolk is about 1:160,000 and in egg white it is approximately 1:87,000 (Surai and Fisinin, 2014). Enrichment of eggs with SeMet due to organic Se dietary supplementation could change those ratios substantially. Since SeMet is not synthesised by animals/poultry it should be provided with the diet. In the egg obtained from the breeders fed on the commercial diet containing about 0.08 mg feed-derived Se/kg, 58-62% Se was found in the egg yolk and 38-42% in the albumin. After supplementing the diet with organic Se at 0.5 mg/kg the Se distribution between egg yolk and albumin was shown to be more equal with 47-48% Se to be found egg albumin (Pappas et al., 2005a). In fact, the efficiency of Se transfer from the diet (at 0.2 ppm supplementation) to the egg was quite high for organic Se sources comprising 56% for Se-Yeast and 76.3% for OH-SeMet (Jlali et al., 2013). It seems likely that efficiency of Se transfer to the egg depends also on the Se form, dose as well as many other factors including chicken genetics, age, etc. For example in another study, at a dosage of 0.1, 0.3, and 0.5 mg/kg Se transfer from feed to the egg was shown to be 43.3; 42.3 and 34.1% for L-SeMet; 36.6; 33.3 and 23.6 for Se-Yeast and 24.0, 23.6 and 16.0% for SS, respectively (Delezie et al., 2014).
In our research trial conducted at the Scottish Agricultural college broiler breeders were fed on the semi-synthetic diet containing 0.044 mg/kg Se and 4.86 mg/kg vitamin E or commercial diet with 0.171 mg/kg Se and 10.05 mg/kg vitamin E. The commercial diet was also supplemented with 0.2 or 0.4 mg/kg organic Se (Se-Yeast). Selenium concentration in the egg yolk increased from 0.30 mg/kg in commercial diet group up to 0.61 and 0.85 mg/kg in Se-Yeast supplemented groups, while Se concentration in egg albumin increased from 0.05 to 0.19 and 0.40 mg/kg in the same groups respectively (Surai, 2000). It seems likely that organic Se (0.3 mg/kg) in the maternal diet can increase GSH-Px activity in the egg yolk and egg albumen (Wang et al., 2010; Rajashree et al., 2014). Interestingly, a sparing effect of dietary Se on vitamin E was observed as evidenced by a significant increase in α-tocopherol concentration in the egg yolk (Surai, 2000). Taking into account a comparatively low vitamin E level in the diet of the control group (10.1 mg/kg) it could be suggested that the sparing effect of Se is mediated by a range of selenoproteins taking part in antioxidant defences and preventing extensive usage of vitamin E. Similar positive effect of dietary Se on vitamin E concentration in the egg was reported later by Skrivan et al. (2008) and Tufarelli et al. (2016).
During incubation Se was transferred from the egg to the embryonic tissues and in the liver of the newly hatched chicks Se concentration increased from 0.38 mg/kg in the control group fed on commercial diet up to 0.73 and 1.4 mg/kg in Se-supplemented groups. Improved Se status of newly hatched chicks was associated with significantly increased GSH-Px activity in the liver of the newly hatched chicks and this difference remained significant at 5 days posthatch (Surai, 2000).
Additional benefit in terms of improvement of antioxidant system of the newly hatched chick comes from significantly increased GSH concentration in the liver due to Se supplementation (Surai, 2000). Interestingly, GSH is one of the most important non-enzymatic antioxidants in animals/poultry participating in redox balance maintenance and signaling, regulation of transcription factors and gene expression and many other important pathways/processes including epigenetic mechanisms (García-Giménez et al., 2017). It was shown that during chicken embryonic development GSH concentration in the liver and brain gradually decreases throughout development, but in the heart and kidney there is a substantial increase in GSH concentration at hatching time (Surai, 1999).
As a result of the aforementioned improvements in antioxidant defence mechanisms lipid peroxidation in the liver of experimental birds at day 1 and day 5 posthatch significantly decreased ultimately reflecting improved resistance to stress (Surai, 2000). As mentioned above hatching process is related to oxidative stress and there are various adaptive mechanisms to deal with such conditions, including increased accumulation of vitamin E and carotenoids, increased GSH-Px activity, etc. However, for the first 10 days posthatch vitamin E in the chicken liver dramatically decreased and this could compromise antioxidant defences at this critical period of chicken ontogenesis when digestive and immune systems are actively developing and desperately need an optimal antioxidant defences/redox balance. Similar to our previous observations (Surai et al., 1997; 1998) in the aforementioned experiment vitamin E concentration in the liver decreased almost 10-fold for the first 10 days of the postnatal development (Surai, 2000). Therefore, significant increase in vitamin E in the chicken liver together with increased GSH concentration and GSH-Px activity due to dietary supplementation of the maternal diet could be of great importance for the growing chicken. Similarly, in comparison to dietary SS supplementation, maternal SeMet supplementation significantly increased the antioxidant status of 1-day-old chicks exhibited by improvement of a range of oxidative stress markers, including increased GSH-Px and SOD activities in breast muscle, enhances kidney GSH concentration, increased T-AOC in breast muscle and liver and inhibited liver and pancreas lipid peroxidation (Wang et al., 2011). Furthermore, it was shown that in comparison to sodium selenite, organic Se sources (Se-Yeast or SeMet) significantly increased the activity of TrxR1 in the liver and kidney, GSH-Px activity and expression of TrxR1 in the liver of progeny chicks (Yuan et al., 2012). Furthermore, compared with SS, both Se-Yeast and SeMet significantly increased the concentration and mRNA level of selenoprotein P1 (SelP1) in day-old chicks (Yuan et al., 2013).
It seems likely that organic Se supplementation to breeders is “an insurance policy” related to investment into the egg Se status to make sure that in stress conditions an optimal protection against over-production of free radicals would be expected. For example, breeders were fed with basal diet (BD) containing 0.04 mg/kg Se or BD supplemented with SS or SeMet at a level of 0.15 mg Se/kg. The rearing experiment lasted for 8 weeks after an 8-week pre-test. Eggs were collected during the last 10-days and incubated in a commercial incubator. On embryonic day 17, fertile eggs were treated with increased temperature (39.5°C) for 6 h. Afterward chick embryos were collected and antioxidant defences were studied (Xiao et al., 2016). The results showed that Se supplementation of the diet of breeders decreased ROS, HSP70, MDA, carbonyl and 8-hydroxydeoxyguanosine (8-OHdG) concentrations and increased GSH-Px, total SOD, and catalase activities in heat stressed chick embryo. It was also shown that ROS, MDA, carbonyl, 8-OHdG concentrations in SeMet treatment group were lower than those in SS treatment. Furthermore, Se supplementation elevated cellular GSH-Px1 mRNA level and activity, cytoplasmic TrxR1 activity and SelP mRNA and protein level. Again, maternal organic selenium showed a higher efficacy than maternal SS in upregulating GPx1, TrxR1, and SelP mRNA levels as well as GPx1 and TrxR1 activities or SelP protein level (Xiao et al., 2016).
Before heat stress, in the liver of 22d turkey embryo there was no difference in HSP70 concentrations between treatments, but GSH-Px activity significantly increased (>2-fold) due to organic Se in the maternal diet. Heat stress was associated with a doubled HSP70 concentration and 1.5-fold increase in GSH-Px activity in the liver of the control group, while there was no response to heat stress from HSP70 in experimental embryos indicating lower stress. However, GSH-Px activity in the embryonic liver of the experimental group significantly increased being 2.4 times higher than that in the control group. Therefore, increased activity of GSH-Px is an adaptive response to heat stress but for that response to be executed there is a need for additional Se which is provided by dietary supplementation of Se in organic form (Rivera et al., 2005).
Therefore, protective effect of Se on breeders is related to building Se reserves in the muscles and making birds more resistant to stress conditions. Secondly improved expression and activities of selenoproteins including GSH-Px, TrxR and SepP substantially contributes to the antioxidant network. Thirdly, increased activities of SOD in breeder’s tissues due to Se supplementation could be an important adaptive mechanism in stress conditions to overcome the excess of free radical production and to re-establish an important equilibrium in the redox status of the cell/tissue/body. Finally, increased expression and possibly concentration of CoQ and other elements of the electron transport chain in the mitochondria could further improve the efficiency of the antioxidant defence system. Regulation of antioxidant systems of the egg is related to increased vitamin E concentration and enhanced GSH-Px activity (Figure 1). Furthermore, protective effect of dietary Se on the newly hatched chick is associated with increased concentrations of vitamin E and GSH, enhanced activities of GSH-Px, TR, SepP and SOD in the liver and/or muscles. Such an improvement of the antioxidant defence network is shown to decrease lipid peroxidation, protein oxidation and DNA oxidation in the liver of the 19-day old embryo exposed to heat stress. Lipid peroxidation also decreased in the newly hatched chicks. Indeed, providing Se in optimal form and in optimal concentration is a key to build the effective antioxidant network in the chicken body responsible for their adaptation to hatching stress and stressful postnatal development.
Long term maternal effect of selenium
For the last few years information has been actively accumulated to indicate that Se in maternal diet could have a long-lasting effect on the antioxidant system of the progeny chicks. First, it was shown that vitamin E concentration in the liver and plasma was significantly elevated in 10-day old progeny chicken due to organic Se (0.2 and 0.4 mg/kg) in the breeder’s diet (Surai, 2000). Secondly, dietary supplementation of the organic Se (0.5 mg/kg) to the maternal quail diet led to a significant increase in Se concentration in the liver, breast, leg and brain of 14 day-old progeny quail (Surai et al., 2006). It seems likely that chicks hatched from high Se eggs has an improved ability to assimilate and metabolise dietary Se. For example, there was a significantly elevated Se level in the liver and breast muscles of the progeny chicks at 3 and 4 weeks posthatch respectively (Pappas et al., 2005b). Taking into account the weight of day old Ross chick (42 g) and 28 days chick (1500g) and breast muscle proportion of about 3% (Zhang et al., 2014a) and 20% (Ross308, 2014) in day old and 28-day old chicks, respectively, there is an incredible (>230-fold) increase in breast muscle mass (from about 1.3 g up to 300 g) for this period of time. If it is taken into account that in the control and experimental birds Se concentration in the muscles at age of 1 day were 56.1 ng/g and 241.3 ng/g respectively and at day 28: 15.4 and 22.6 ng/g, respectively. Therefore, the total Se amount in breast muscle (Se reserves) of day old chicks would be 72.9 ng and 313.7 ng, and 240.8 ng difference in day old chicks and 4620 ng and 6780 ng, an 2160 ng difference at day 28. In fact, a difference is almost 2,000 ng per chick confirming that Se transferred from the egg to the newly hatched chicks and Se in the chicken muscles at age of 28 days is not the same Se, growing chicks in the experimental group applied almost 2000 ng extra Se from the feed for this period of time (Pappas et al., 2005b). Similarly, in comparison to a non-supplemented diet containing 0.13 mg Se/kg, organic selenium (0.3 mg/kg) in the maternal diet for 4 weeks was responsible for increased Se concentration, decreased lipid (MDA) and protein (carbonyls) oxidation in muscles of 21-d old progeny chicks and improved a water holding capacity of the meat (Wang et al., 2009). Furthermore, in comparison to SS dietary supplementation, maternal Se-Met supplementation (0.3 mg/kg) was shown to significantly improve the FCR of the offspring during 56 day growth and significantly decreased the mortality of the chicks during the first week posthatch and 8-week growing period (Wang et al., 2011). Interestingly, SeMet breeder supplementation improved hatchability (90.8 vs 85.1) as well. In continuation of this study it was shown that in comparison to SS supplemented breeder diet, SeMet in maternal diet (0.3 mg/kg) for 8 weeks was responsible for a significantly increased Se concentrations in serum, liver, kidney, and breast muscle of the 56-d-old offspring chickens. In contrast with maternal SS supplementation several indexes of antioxidant defence in a progeny chicks obtained from breeders supplemented with SeMet were also improved including increased GSH-Px activity in serum and breast muscle, GSH concentration in serum, and total antioxidant capability in pancreas, as well as cytosolic GSH-Px mRNA abundance in breast muscle, liver, and pancreas (Zhang et al., 2014b). Interestingly, the maternal Se-Met treatment was shown to be associated with a significant reduction of the 48-h drip loss of 56-d-old progeny chickens in comparison with maternal SS treatment.
Commercial applications of dietary Se
Generally speaking beneficial effect of dietary Se on breeder’s performance would depend on the level on stress where additional antioxidant protection is required.For example,inclusion of omega-3 PUFAs into the breeder diet could be an important nutritional stress for the breeders and developing embryos. In particular, some aspects of egg quality such as Haugh Units are adversely affected by egg storage and dietary fish oil. In fact, maternal Se supplementation (0.5 mg/kg) was shown to slow down Haugh Units deterioration after 14 d of storage of eggs enriched with omega-3 fatty acids (Pappas et al., 2005a). In another experiment conducted at the Scottish Agricultural College, the control breeders were fed on diet containing <0.1 mg/kg of Se, while experimental breeder diet was supplemented with organic selenium at 0.5 mg Se/kg (Pappas et al., 2006a). A protective effect of dietary Se was shown when fish oil (a dietary stress factor) was included in the breeder diet and increased embryonic mortality in wk 3 of incubation and reduced hatchability and weight of 1-d-old chick observed. In fact, the addition of Se to the FO-enriched diets was found to ameliorate some of the aforementioned adverse effects (Pappas et al., 2006a).
There is a range of publications showing beneficial effects of Se on breeder and layer performance. For example, protective effects of selenium on production and reproduction performance of heat-stressed poultry has been recently summarized (Habibian et al., 2015). Furthermore, at 0.3 ppm supplementation there was no difference between SS, Se-Yeast or SeMet in relation to their effect on egg production, fertility or hatchability, but at 0.15 ppm breeders fed on SeMet showed a significant increase in egg production in comparison to SS or Se-Yeast (Yuan et al., 2011). A 10-week experiment was conducted with Ross 308 broiler breeder chickens in cages to evaluate the influence of organic and inorganic sources of supplementation (Rajashree et al., 2014). A total of 600 birds at 29 weeks of age were divided into 4 groups and fed on a maize-soya basal diet supplemented with different forms of Se. The first (control) group was given the basal diet without Se supplementation, whereas the second, third and fourth groups were given, respectively, the basal diet with 0.3 mg/kg of inorganic Se in the form of SS or 0.3 and 0.5 mg/kg of organic Se in the form of Se-Yeast for 10 weeks. At the end of the experiment (39 weeks), there was a reduction in mortality in breeders fed on the diet supplemented with 0.5 mg/kg of organic selenium. In addition, organic Se at 0.5 mg/kg increased egg production, percentage of settable eggs and hatchability (Rajashree et al., 2014). In fact the birds fed an organic Se supplemented diet (0.3 mg/kg) was associated with increased number of settable eggs, improved fertility, hatch of fertile eggs, hatchability, A-grade chicks and reduced embryonic mortality in comparison to breeders fed inorganic selenium or non-supplemented diet (Khan et al., 2017).
However, when balanced diet and well-controlled conditions are used in most cases the form and concentration of dietary Se do not affect breeder performance (Surai, 2000; Paton et al., 2002; Jing et al., 2015; Urso et al., 2015) or layer performance (Jiakui and Xialong 2004, Payne et al., 2005; Chantiratikul et al. 2008; Bennett and Cheng, 2010; Scheideler et al., 2010; Pavlovic et al., 2010; Mohiti-Asli et al. 2010; Pan et al., 2011; Jlali et al., 2013; Tufarelli et al., 2016).
Selenium is shown to be an effective modulator of the antioxidant systems in poultry. From the one hand, Se is involved in expression and synthesis of 26 selenoproteins, including GSH-Px, TrxR and SepP. In fact, more than half of known selenoproteins are directly or indirectly involved in antioxidant defences and redox status maintenance. On the other hand, Se affects non-enzymatic (vitamin E, CoQ and GSH) and enzymatic (SOD) antioxidant defence mechanisms helping build a strong antioxidant defences in breeders, developing embryos and newly hatched chicks. Long term maternal effects of dietary Se need further investigation. It is clear that Se efficiency depends on the level of supplementation and form of dietary Se. For example, sodium selenite, a common Se dietary supplement, is not effective in increasing Se concentration in the egg and embryo and therefore has a limited ability to modulate antioxidant system of the developing embryo and newly hatched chicks. Indeed, organic Se sources are proven to be more effective modulators of the antioxidant systems in poultry. Our previous analysis (Surai and Fisinin, 2014) has shown that among organic Se sources, OH-SeMet has the greatest potential/ability to enrich the egg with Se (Jlali et al., 2013) and therefore to affect antioxidant defences of the developing chicken embryo. In fact, our analysis of composition of eggs collected from various avian species in wild (UK and New Zealand) showed that Se level in those eggs are close to the levels found in commercial chicken eggs after 0.3 ppm organic Se supplementation (Pappas et al., 2006b). However, a recently introduced restriction in EU related to maximum organic Se supplementation of poultry/animal diets at 0.2 mg/kg, makes OH-SeMet a supplemental Se form of choice to meet Se requirement of commercial poultry. It seems likely that antioxidant/prooxidant (redox) balance of the gut (Surai and Fisinin, 2015) and the role/interactions of Se and microbiota in maintaining gut health (Surai et al., 2017) would be a priority for future research. In the second part of the review nutritional modulation of the antioxidant defence system with vitamin E and carotenoids will be considered.
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Figure 1. Antioxidant system modulation by dietary selenium
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