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METABOLISM AND NUTRITION |
Avian Science Research Centre, Animal Health Group, Scottish Agricultural College, West Mains Road, Edinburgh EH9 3JG, UK
1 Corresponding author: Regina.McDevitt{at}sac.ac.uk
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Key Words: selenium • polyunsaturated fatty acid • breeder age • incubation • hatchability
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The yolk is the primary source of energy and nutrients for the embryo during its development. The energy needs of the embryo throughout the 21-d developmental period of incubation are obtained by the ß-oxidation of the fatty acids (FA) derived from the yolk lipids (Speake et al., 1998b). Furthermore, yolk lipids are the source of FA and other components needed for the synthesis of membrane phospholipids in the growing tissues of the embryo. The increased mortality displayed by embryos from young broiler breeders (25 wk old) is associated with a pattern of lipid transfer that is significantly different from that of the embryos of 45-wk-old breeders when production is at peak levels (Noble et al., 1986). A lower proportion of the total yolk lipid was transferred into embryos from 25-wk-old hens by d 19 of incubation, compared with embryos from 41-wk-old hens, because the lipid was still associated with the yolk (Noble et al., 1986; Yafei and Noble, 1990). The embryo from the younger hen, therefore, may have reduced access to its major energy source and the essential nutrients that the yolk lipid contains (Noble et al., 1986; Yafei and Noble, 1990). Changes in the profile of yolk FA with hen age have also been reported. Scheideler et al. (1998) reported that 36-wk-old broiler breeders laid eggs with a reduced concentration of doco-sahexaenoic FA (DHA) compared with those laid by 58-wk-old hens. Similarly, newly hatched ducklings from 24-wk-old breeders had lower concentrations of linoleic acid (C18:2n-6) in the liver compared with ducklings originating from 31-wk-old breeders (Braun et al., 2001). Certain tissues of the developing chick embryo, in particular the brain and retina, require a high concentration of poly-unsaturated FA (PUFA), such as DHA. The embryo has evolved a sophisticated antioxidant defense system to protect these tissues from the effects of oxidation (Speake et al., 1998a).
The role of Se as an antioxidant has been reviewed extensively (Surai, 2002a,b). Selenium can be added to the diet as selenite or selenate (inorganic) or as organoselenium compounds (selenoamino acids, mainly selenomethionine). Although it has been shown that Se can be transferred from the maternal diet to the hatching egg and to the embryo, these studies tend to focus on the incorporation of Se into the albumen and yolk (Surai, 2000; Paton et al., 2002; Pappas et al., 2005). Although there is evidence that Se, like other trace elements, is present in the eggshell (Richards, 1997), there are few reports that detail whether dietary supplementation of parent diets can affect the concentration of Se in the eggshell (Surai et al., 2004). If Se is located in the cones of the shell, and, in particular, that area of the cone associated with the mammillary core and shell membranes (as is the case for magnesium; Board and Love, 1980), Se in the eggshell could provide an additional route for enhancing the Se content of the embryo. If Se is resorbed from the shell, the antioxidative status of the embryo could be enhanced and provide protection during hatching, which is known to be a time of increased oxidative stress for the embryo.
The present study was part of a project designed to assess the effect of the inclusion of PUFA and Se in the maternal diet on embryo viability, hatchability, and the subsequent growth of the progeny. In our previous work, we evaluated how these nutrients affect the egg quality, in particular, internal egg quality during storage as well as the concentration of Se in the yolk and albumen of freshly collected eggs (Pappas et al., 2005). The aim of the present study was to assess the effect of the inclusion of PUFA and Se in the maternal diet, which may protect the PUFA from oxidation, on the developing embryo and the newly hatched chick. In addition, we reported on the concentration of Se in the eggshell of these eggs. Therefore, the embryonic mortality and hatchability of eggs, as well as hatching chick BW, of prepeak (23 wk) and peak (27 wk) production broiler breeders that had been fed diets with and without supplemental Se and PUFA was assessed.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Details of the genotype, nutrition, and husbandry of the broiler breeder used in the present study have been described previously (Pappas et al., 2005). In brief, a total of 352 Hubbard-ISA broiler breeders were reared in 16 pens of 22 birds each, with a ratio of 1 male to 10 females, in an environmentally controlled facility. The Animal Experiments Committee of the Scottish Agricultural College approved the design and conduct of this study. There were 4 replicates of 4 dietary treatments: a commercial broiler breeder diet with soybean oil (SO) or fish oil (FO; United Fish Industries Ltd., Grimsby, UK), but no added Se, and each diet with added Se as Sel-Plex (SO + Se, FO + Se; Alltech Biotechnology, Nicholasville, KY). The birds were fed (restricted feeding) a grower diet to wk 20 of life, and from wk 21 they were fed a breeder diet (Table 1
) according to Hubbard-ISA’s management manual. In addition, water was provided ad libitum. Prior to the study, the wheat, soybean meal, and oat hulls that comprised the basal diet were analyzed for their Se content, which was 0.037, 0.084, and 0.024 mg/kg, respectively (dietary requirement is 0.1 mg/kg; National Research Council, 1994). Based on this information, the diets were designed to contain >0.1 mg/kg for the nonsupplemented treatment (no added Se), and the intended supplemented level of Se was 0.5 mg/kg. The diets were analyzed for lipid content, which was 65 g/kg for all treatment groups. This comprised 55 g/kg of added oil, either SO or FO, and an additional 10 g/kg of lipid supplied from the other dietary ingredients. However, the FA profile of the diets differed in that SO was used in 2 of the treatments (SO and SO + Se), and FO was used in the other 2 diets (FO, FO + Se). The n-6:n-3 ratio of the diets containing SO and FO was determined to be 11.5 and 1.7, respectively (Table 1).
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The hatching eggs that were collected at each hen age were divided into 2 groups; 1 group was used to determine the effect of parental treatment on various parameters during egg storage (Pappas et al., 2005), and the second group of eggs was incubated for use in the current study. Hatching egg weight was determined in the eggs used for the storage study only (Pappas et al., 2005), and any correlations between 1-d-old chick BW and hatching egg weight refer to the weight of eggs that were collected for the storage study (egg weight at d 0 of storage study). The destruction of eggs was required for the determination of Se in the eggshell, and, therefore, these eggs did not go through the process of incubation. The hatching eggs were opened on the day of collection, and the contents (yolk and white) were removed. The eggs were then rinsed with distilled water, dried in an oven (65°C) to a constant mass, and eggshell weight was recorded.
Candling was performed on d 7 and 19 of incubation, and a breakout analysis of dead embryos was performed to assess the age at which embryonic mortality occurred. Embryonic mortality that occurs during the first week of incubation is characterized by the presence of blood islands (groups of mesodermal cells, 1 of the 3 germ layers in the early developing embryo, from which immature erythrocytes develop) and the absence of eyes (Christensen, 2001; Ruiz and Lunam, 2002). Embryonic deaths of this kind usually occur between d 0 and 4 of the start of incubation (Ruiz and Lunam, 2002). The embryos that die during wk 2 are characterized by the presence of both eyes and feathers (Ruiz and Lunam, 2002). The last category included the deaths that took place during wk 3 of incubation, which were characterized by the embryo occupying the entire inner-egg space (Ruiz and Lunam, 2002). These deaths usually occurred between d 18 and 22 of the incubation, and, in most cases, the residual yolk was not drawn into the abdominal cavity. Embryos that died during pipping or were found dead on the hatching tray were categorized as deaths during wk 3 of incubation.
At hatch, 4 chicks were randomly selected from each parental treatment replicate (which had been kept separate by pedigree cans) and weighed, so that BW was obtained in 16 randomly selected chicks per treatment (4 chicks per replicate x 4 pens per treatment). The Se concentration and FA profile of brain and liver tissues was determined in 8 chicks per treatment, 2 per replicate, at hatch.
Analytical Procedures
Total lipid content was extracted from the brain and liver using the method of Noble et al. (1990). The mass of total lipid content was determined gravimetrically. The FA methyl esters were analyzed by gas-liquid chromatography using a capillary column (60 m x 0.22 mm inside diameter, coated with BPX70 with a film thickness of 0.25 µm, SGE, Cairns, Australia) in a CP9001 instrument (Chrompack, Middleburg, The Netherlands) connected to an EZ Chrom data system (Scientific Software Inc., San Ramon, CA) to determine the FA profile of the lipid. The identification of the peaks was confirmed by comparison with an external standard of a mixture of FA methyl esters (Sigma-Aldrich, Gillingham, Dorset, UK).
Selenium concentrations were determined using hydride generation atomic fluorescence spectroscopy of the acid digest of the samples (Surai, 2000). The method used a hydride generator, a fluorescence detector (model 10·033, PS Analytical Ltd., Kent, UK) fitted with a boosted discharge hollow cathode lamp (superlamp Se, Photon, PTY Ltd., Crows Nest, Australia), an autosampler (model 20·099, PS Analytical Ltd.) and Avalon (model 20·099, PS Analytical Ltd.) software.
Statistical Analyses
The data were analyzed statistically using Genstat (Version 7, VSN International Ltd., Herts, UK). All variates were analyzed by ANOVA with block and pen as random factors. Three factors were examined: Se supplied in the broiler breeder diets at low or high levels; n-3 FA at low or high levels; and eggs from hens at 23 or 27 wk of age. All interactions (Se by oil by age) were analyzed, and all pairwise comparisons were tested. The data for interactions among the 3 main terms of Se, PUFA, or breeder age are only presented when significant interactions occurred. Percentage data, such as those of embryonic mortality or FA, underwent angular transformation prior to analysis. The angular transformation was applied to the data to satisfy the ANOVA assumption of homogeneity of variances (equal variances). Data for Se concentration in the tissues were not normally distributed, and, therefore, were log-transformed prior to analysis. Means and SE are presented on the original scale. The data are presented as mean ± SEM. Statements of significance were based on P < 0.05, unless otherwise stated.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The age of the laying hen significantly affected the number of fertile eggs laid. The fertility of eggs (i.e., the number of fertile eggs as a percentage of the total number of eggs incubated) laid by 27-wk-old hens (pooled from all dietary treatments) was greater compared with eggs laid by 23-wk-old hens (Table 2). As would be expected, embryonic mortality (i.e., the number of eggs with dead embryos as a percentage of the number of fertile eggs) was, irrespective of parent age, higher during the first and last week of incubation when compared with wk 2 of incubation (Table 2). The embryonic mortality during wk 1 of incubation decreased as the age of the hen increased from 23 to 27 wk. The oil source and the supplementation of the broiler breeder diet with Se did not affect embryonic mortality during wk 1 of incubation. There was no effect of dietary treatment or parental age on mortality during wk 2 of incubation. However, during the last week of incubation, embryonic mortality was lower in eggs laid by 27-wk-old hens compared with those laid by 23-wk-old hens. In addition, FO significantly increased embryonic mortality during wk 3 of incubation. Embryonic mortality during wk 3 in eggs laid by all hens fed FO (FO and FO + Se) was 2 times higher than that of eggs laid by all hens from the SO treatments (SO and SO + Se). Supplementation of the hen diets with Se did not affect the embryonic mortality during the third week.
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). The use of FO in the broiler breeder diet resulted in lower hatchability compared with the hatchability of eggs from hens fed diets containing soybean oil, irrespective of the Se level in the diet. Hatchability was greater in 27-wk-old hens compared with 23-wk-old hens, and supplementation of the hen diets with Se did not affect hatchability.
Supplementation of the maternal diet with FO reduced BW at hatch by about 6% compared with that of chicks from hens fed diets containing SO (Table 3). Selenium supplementation of the maternal diet ameliorated some of the adverse effects of FO supplementation. Chicks from the 23-wk FO + Se hens were 1 g heavier than those of the 23-wk FO-treatment hens. However, this effect was not observed in eggs laid by 27-wk-old hens from the same treatment groups. There were no differences in BW at hatch of chicks from the SO and the SO + Se hens, irrespective of hen age. Hen age had a positive effect on chick weight, because those hatched from eggs laid by 27-wk-old hens (pooled for all dietary treatments) were 4 g heavier than those hatched from eggs laid by 23-wk-old hens, irrespective of dietary treatment.
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Selenium supplementation of the maternal diet resulted in a 3-fold increase in the concentration (nanograms per gram) of Se in the eggshell (Table 4). This increase was independent of both the level of PUFA in the diet and the age of the hen. Similarly, the amount (concentration x shell weight, nanograms) of Se present in the eggshell of hens fed the high-Se diets (SO + Se and FO + Se) increased by a factor of 3 compared with the amount present in the shell of eggs laid by hens fed the low-Se diets. The amount of Se in the eggshell increased as the age of the hen increased from 23 to 27 wk.
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). There were no differences in the Se concentration of brain and liver in chicks hatched from eggs laid by hens fed either of the 2 high-Se treatments (FO + Se, SO + Se). This observation was consistent for chicks from breeders of both ages. However, in the 23-wk-old hens, Se concentrations in the brains of chicks from FO hens were significantly higher than that from the SO hens. Overall (pooled to include data from both hen ages), the oil source had a significant effect on Se concentrations in the brain and liver, with chicks from the FO hens having higher Se concentrations than chicks from the SO hens. The concentration of Se in the brain of chicks from 27-wk-old breeders was lower than that found in chicks from 23-wk-old hens. The oil source affected the Se concentration in the liver, because chicks from the FO treatment had higher Se concentration in the liver than that of chicks from the SO treatment. There was a significant interaction between parental age and dietary Se in the liver; chicks from 23-wk-old hens fed FO had higher Se in the liver compared with SO, but there was no difference in the concentration of Se in the liver of chicks from SO and FO treatments in 27-wk-old hens.
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The brains of chicks from hens fed the FO treatments had lower total lipid content, higher concentrations of n-3 FA, lower concentrations of n-6 FA, and, consequently, had lower n-6:n-3 ratios compared with those from hens fed the SO treatments (Table 6). The brains of chicks from 23-wk-old hens fed SO (SO and SO + Se treatments) contained more lipids than that of chicks from hens fed FO (FO and FO + Se). However, these differences were not noted in chicks from 27-wk-old hens, in which chicks from all treatments had similar lipid content. Selenium supplementation of the parental diet had no effect on the total lipid content of the chick brain, irrespective of parental age. There were no differences in the brain FA profiles of chicks originating from the FO and FO + Se treatments or the SO and SO + Se treatments, irrespective of hen age. However, there was a tendency (P = 0.08) for the DHA (C22:6n-3) concentration to be higher in the brain of chicks from breeders fed diets supplemented with Se.
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). The livers of chicks from 27-wk-old breeders had higher lipid contents than that of chickens from 23-wk-old breeders. There were higher concentrations of n-3 FA, lower concentrations of n-6 FA, and, consequently, a lower n-6:n-3 ratio in the liver of chicks from breeders fed FO compared with those from hens fed the SO treatments. The FA profiles of livers from chicks from hens fed FO diets were the same regardless of Se supplementation. However, the livers of chickens from the breeders fed the SO + Se diets had higher concentrations of DHA, compared with the concentration of DHA in the livers of chicks from breeders of the SO treatment. Consequently, the hepatic n-6:n-3 ratio was lower in these birds. Overall, Se had a positive effect on the hepatic concentration of DHA, as chicks hatched from breeders fed Se had higher concentrations of DHA in their liver compared with chicks from breeders fed the low-Se treatments.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The transfer of Se from the hen diet to the eggshell has been demonstrated in quail (Surai et al., 2004). Several other elements (Zn, Cu, Fe, and Mn) have been shown to be transferred from chicken breeder diets into the membranes and shell of the egg (Richards, 1997; Miles, 2000). The amount of Se that could potentially be resorbed by the embryo from the eggshell will be determined in part by the distribution of Se within the shell and associated membranes. During embryogenesis, the embryo will resorb Ca and, to a lesser extent, other elements from the shell that opposes the shell membranes (i.e., the tips of the mammillary layer). Approximately 120 mg of Ca or 5% of the total shell Ca by weight is resorbed during this process (Tuan, 1987). If the Se is distributed evenly throughout the eggshell, then only the amount that is present in the mammillary layer of the shell can potentially be resorbed by the embryo. Thus, on the basis of the data in the present study, the amount of Se available for resorption will be about 3 ng for the low-Se treatments and about 9 ng for the high-Se treatments. However, from previous studies (Tuan, 1987; Wadell et al., 1987), it is likely that the Se is not distributed evenly throughout the shell but may be concentrated in the mammillary or surface crystal layer or both. If this is correct, then a greater quantity of Se (from 50 to a maximum of 200 ng, depending on the dietary treatment) may be resorbed by the embryo during embryogenesis, though it is unlikely that the maximum possible amount of Se would be resorbed. This would be the equivalent to ~1 to 2% of the Se that may be utilized from the egg contents and is unlikely to have a significant effect on the embryo per se. However, it may influence the ultrastructure of the shell or the resorption characteristics of the calcite (Stoewsand et al., 1978; Klecher et al., 1997; Paton et al., 2000).
The relationship between reduced fertility and increased embryonic mortality in hens of different ages has been well described (Noble et al., 1986; Ruiz and Lunam, 2002) and was observed in the present study. Fairchild et al. (2002) suggested that changes in sperm storage tubules might alter the number of sperm that can be stored, and less than optimal sperm numbers could contribute to a negative correlation between fertility and early embryonic mortality. Alternatively, poor fertility might be because the phospholipids of avian spermatozoa are characterized by high proportions of arachidonic and docosate-traenoic FA, which are very susceptible to oxidation. Studies in which male breeder diets have been supplemented with menhaden oil (rich in PUFA) have resulted in positive effects on fertility and sperm quality (Hudson and Wilson, 2003). In addition, supplementation of male breeder diets with 0.3 mg/kg of Se increased glutathione peroxidase (GSH-Px) activity and enhanced protection against lipid peroxidation in the cockerel semen (Surai et al., 1998). It might, therefore, be expected that supplementation of the broiler breeder diets with Se would influence the fertility of the eggs, by protecting the PUFA component of the semen, but this was not the case.
Long-chain n-3 PUFA are very important for a range of physiological functions in the avian metabolism such as eicosanoid metabolism and immune-related functions (Watkins, 1991), development of the central nervous system and brain (Lauritzen et al., 2001), and in lipid metabolism (Cherian and Sim, 2001; Newman et al., 2002). Therefore, modifying breeder diets to increase the level of n-3 PUFA by using FO might be expected to improve, or at the very least, not adversely affect breeder performance. Indeed, Karrick (1990) found that supplementing the diets of hens with FO had a positive effect on egg production, fertility, and hatchability, whereas Anderson et al. (1989) found that FO supplementation had no adverse effect on breeder performance. In contrast, the levels of FO used to supplement the broiler breeder diet in the present study negatively affected embryonic mortality during wk 3 of incubation and reduced the hatchability of eggs from the 23-wk-old hens. Furthermore, at hatch, the BW of chicks from hens fed diets that contained FO was reduced compared with that of chicks hatched from hens fed diets containing SO. The cause of the higher mortality in the FO treatment may be due either to the high level of PUFA and the associated increase in free radicals generated or may simply reflect physical constraints arising from the smaller eggs laid by these hens. Some PUFA, like those found in FO, are involved in gene transcription, with PUFA upregulating the expression of genes encoding proteins involved in FA oxidation and simultaneously down-regulating genes encoding proteins of lipid synthesis (Clarke, 2001). An increased supply of PUFA interferes with the synthesis of very low density lipoproteins in rats (Lang and Davis, 1990). Because very low density lipoproteins are the precursors for egg yolk lipids, this may be the mechanism that resulted in eggs with smaller yolks, smaller eggs, and, consequently, led to smaller-sized embryos and lightweight 1-d-old chicks when FO was fed to hens (Pappas et al., 2005). The chicks in the present study that were hatched from hens fed diets containing FO were approximately 2 g lighter than chicks from hens fed diets containing SO, which supports this hypothesis. The lighter BW of chicks from the FO treatments is directly attributable to a lighter hatching egg. Hatching BW was 66% of the hatching egg weight, confirming previous reports (Tullett and Burton, 1982; Shanawany, 1987; Wilson, 1991). Selenium had a positive effect on BW, as chicks hatched from eggs laid by 23-wk-old hens of the FO + Se treatment were heavier than those hatched from the FO treatment. It is believed that this effect of Se was due to amelioration of some of the adverse effects of FO supplementation, as there were no differences in BW between chicks hatched from hens of SO and SO + Se treatments. Previously, a reduction in egg weight due to the addition of FO to breeder hen diets was not so pronounced when Se was also added to the hen diet (Pappas et al., 2005). Chick weight increased with increasing parent age and egg weight (Shanawany, 1984; Bruzual et al., 2000a; Braun et al., 2002b), and this effect was even seen in hens that had been fed FO.
It is well established that embryo livability and hatchability improve as the age of the hen increases (Roque and Soares, 1994; Suarez et al., 1997; Burnham et al., 2001; Christensen, 2001; Christensen et al., 2001; Peebles et al., 2001; Tona et al., 2001; Braun et al., 2002b). Embryonic mortality during wk 3 in the present study was reduced by half, and hatchability increased from 67.3 to 88.9% as the age of the hen increased from 23 to 27 wk. These changes in embryonic mortality and hatchability of fertile eggs with parental age can be attributed, but not limited to, changes in egg size (Burnham et al., 2001), shell characteristics (Peebles and Brake, 1987; Roque and Soares, 1994), reduced mobilization of yolk lipid by the embryo, and an altered FA profile (Yafei and Noble, 1990; Braun et al., 2002a).
At hatching, chicks from hens fed FO had higher concentrations of n-3 FA, lower concentrations of n-6 FA, and, consequently, had a lower n-6:n-3 ratio compared with those from hens fed the SO treatments. For all treatments, the n-6:n-3 ratio in the brain of newly hatched chicks was lower than that measured in the liver. This result confirms previous reports that the brain is the target tissue of n-3 PUFA metabolism (Speake et al., 1998b). The brain and retina are known to require large amounts of DHA (Anderson et al., 1989; Lauritzen et al., 2001), and, usually, the proportion of DHA in the phospholipids of these tissues is far higher than the original yolk phospholipid levels. Thus, the embryo must have some mechanism for increasing the concentrations of DHA in the tissues beyond what is supplied from the yolk. This bio-magnification of PUFA levels in embryonic tissues is believed to be mediated by the yolk sac membrane (Speake et al., 1998b).
The concentration of DHA was increased in the liver of chicks from the SO + Se treatment compared with that of chicks from the SO treatment, even though neither diet contained FO. A similar response was observed in the DHA content of hatching eggs from parents fed the same diets (Pappas et al., 2005). Thus, Se and PUFA may interact not only at the level of hatching egg but during embryogenesis as well. There was evidence of further interactions between Se and PUFA, as the concentration of Se in the brain and liver of chicks from hens fed a diet containing FO was greater than that measured in chicks from hens fed the diet containing SO, despite the fact that both groups of chicks originated from parents fed the same diet that was low in Se. The interaction between Se and PUFA may occur through the action of selenoenzymes with antioxidative functions, such as Se-dependent GSH-Px. Glutathione peroxidase has been reported to play an important role in regulation of the biosynthesis of prostaglandins from their precursor FA, arachidonic acid (Hong et al., 1989). Furthermore, recent studies revealed that feeding rats a diet deficient in Se significantly reduced the concentration of some PUFA, for example, DHA, and increased the concentration of some n-6 FA (Schafer et al., 2004). The involvement of Se in the modulation of lipid metabolism could be through direct effects of Se on the antioxidant defense, as well as through indirect effects on the desaturation and absorption of FA (Schafer et al., 2004).
The level of Se in the hatching egg (Surai, 2000; Paton et al., 2002) and whether the Se is in an inorganic form or part of an organic molecule (Paton et al., 2002) will influence the amount of Se transferred to the developing embryo and the 1-d-old chick. The nutritional status of the laying hen will determine the efficiency of the antioxidant system throughout embryonic and early postnatal development of the offspring (Surai, 2000). Selenium supplementation in the organic form (e.g., selenomethionine) results in higher concentrations of Se in tissues than when Se in an inorganic form is used (Whanger, 2001; Paton et al., 2002). In this study, the concentration of Se in the brain of 1-d-old chicks was lower than the concentration of Se in the liver of the same chicks, which may be due to a unique metabolism of Se by the brain, as has been suggested by Whanger (2001). Whanger (2001) suggested that Se does not affect GSH-Px activity in the brain to the same extent as in other organs, and that vitamin E has a greater antioxidant effect than Se in reducing lipid peroxidation in various brain regions. This may indicate that a combination of Se and high levels of vitamin E in the present study might have further protected the PUFA in the developing embryo. Indeed, a combination of dietary Se supplementation with high vitamin E levels has been shown to further increase GSH-Px activity in the liver of chickens compared with that of Se supplementation alone (Surai, 2000).
The present study demonstrated that there were significant interactions between Se and PUFA supplementation in the maternal diet and the level of Se and PUFA in the tissues of the newly hatched chick. The fertility, embryonic livability, and hatchability of the hatching eggs increased with hen age and production level, as would be expected. However, the inclusion of high levels of PUFA in the broiler breeder diets can adversely affect embryonic mortality, hatchability, and chick BW at hatching. This study demonstrated that the addition of organoselenium compounds to the maternal diet can ameliorate the adverse effects of high levels of PUFA on hatching chick BW.
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ACKNOWLEDGMENTS |
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Received for publication November 21, 2005. Accepted for publication March 27, 2006.
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