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METABOLISM AND NUTRITION |
Avian Science Research Centre, Animal Health Group, Scottish Agricultural College, West Mains Road, Edinburgh, 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: broiler • docosahexaenoic acid • selenium • polyunsaturated fatty acid
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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-linolenic acid had higher concentrations of circulating Ig G compared with chicks hatched from hens fed diets with a high ratio of linoleic to -linolenic acid (Wang et al., 2004). Thus, the addition of the n-3 and n-6 series of PUFA to the maternal diet affects the passive immunity of the progeny (Wang et al., 2004). Supplementation of broiler breeder diets with fish oil (FO) can influence the brain docosahexaenoic acid (DHA) content of progeny fed a diet deficient in DHA, which can last for up to 6 wk posthatch (Ajuyah et al., 2003). The same authors concluded that, considering the role of DHA in early brain development, the maternal supply of DHA might be of importance when chicks are fed a DHA-deficient diet. Furthermore, the mineral content of the maternal diet has also been shown to affect the progeny. For example, Dylewski et al. (2002) reported that neonate rats nursed by mothers fed a diet with low levels of Se had lower levels of T cytotoxic cells, natural killer cells, and B cells than neonates nursed by mothers fed adequate Se in the diet. These results indicate that adequate Se in the maternal diet is important for proper development and function of the immune system of the neonate rat. Obviously mammalian neonates have a constant access to maternal nutrients throughout lactation, whereas avian embryos and chicks rely on adequate amounts of nutrients being deposited in the egg by the hen prior to oviposition. Surai (2000) fed broiler breeders with diets that were not supplemented with vitamin E and Se or were supplemented with Se (organo-Se compounds), vitamin E, or both nutrients. The egg yolk and the liver of the 1-d-old chick that originated from breeders fed the diets supplemented with Se had increased concentration of vitamin E compared with that found in the egg yolk and liver of chicks from the nonsupplemented treatment, indicating that Se may have a sparing effect on vitamin E metabolism (Surai, 2000). The age and production level of the broiler breeder also has an effect on the nutritional status of the progeny. Circulating levels of lipoproteins (Braun et al., 2002a) and the proportion of unabsorbed yolk lipid (Yafei and Noble, 1990) are lower in embryos from young (~20 wk) breeder ducks and broiler breeders, respectively, compared with older (35 to 40 wk) parents of either species. In addition, ducklings hatched from 24-wk-old breeders had a lower body mass and a higher mortality rate compared with ducklings hatched from 31- or 47-wk-old parents (Braun et al., 2002b).
The present study was part of a project designed to assess the effect of the inclusion of PUFA and Se in the diet of broiler breeders on egg quality, embryo viability, hatchability, and the subsequent growth and performance of the chick progeny during the early part of the life. Previously, we evaluated how these nutrients affected the egg quality, and in particular, internal egg quality during storage (Pappas et al., 2005). Furthermore, we assessed how these nutrients affect hatchability (Pappas et al., 2006). The aim of the present study was to assess the effect of the inclusion in the maternal diet of PUFA and Se on the nutritional status and growth of the progeny. Therefore, growth, performance, mortality, and tissue concentration of Se and PUFA were assessed in the progeny of breeders fed diets with or without supplementary dietary Se and PUFA inclusion.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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) according to Hubbard-ISA’s management manual, and water was provided ad libitum (Pappas et al., 2005). Prior to the study, the wheat, soybean meal, and oat hulls that comprised the basal diet were analyzed for their Se content (0.037, 0.084, and 0.024 mg/kg, respectively). The dietary requirement for broiler breeders is 0.1 mg/kg (NRC, 1994). Based on this information, the diets were designed to contain less than 0.1 mg/kg for the nonsupplemented (no added Se) and about 0.5 mg/kg for the supplemented diets since this is the upper recommended concentration of Se in the diets of poultry. The lipid content of the diets was similar (65 g/kg) for all treatment groups. However, the fatty acid (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 chicks were fed diets of differing nutrient density to place one treatment group under nutritional stress and therefore exacerbate the potential effects of parental treatment on progeny performance. Feed and water were provided ad libitum. In both diets, the vitamins and minerals were supplied to meet the nutritional requirements of the chicks; thus the Se content of each diet was about 0.2 mg·kg–1 Se in the form of sodium selenite [dietary requirement is 0.15 mg·kg–1 (NRC, 1994)]. The lipid content of the diets was 65 g·kg–1 for the HQ diet and 52 g·kg–1 for the LQ diet, respectively. The n-6/n-3 ratio for both diets was 12.0. At 0, 7, and 14 d posthatch, the chicks and feed were weighed, from which weight gain and feed conversion ratio (FCR) were calculated. At the same intervals, a chick was randomly selected from each cage for the determination of Se and FA profiles. Of these 8 chicks, 4 were used for determination of Se and 4 were used for FA analysis. The broiler chicken growth study was conducted with the same number of chicks hatched from eggs laid by 27-wk-old breeders.
Analytical Procedures
Total lipid was extracted from the egg yolks using the method of Noble et al. (1990). The mass of total lipid was determined gravimetrically. The FA methyl esters were analyzed by capillary (60 m x 0.22 mm inside diameter, coated with BPX70 with film thickness of 0.25 ·m, SGE, Cairns, Australia) gas-liquid chromatography in a CP9001 instrument (Chrompack, Middleburg, the Netherlands) connected to an EZ Chrom Data System (Scientific Software, 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 FA methyl ester mixtures (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 10ª033, PS Analytical Ltd., Kent, UK) fitted with a boosted discharge hollow cathode lamp (Superlamp Se, Photon, PTY Ltd., Australia), an autosampler (Model 20·099, PS Analytical Ltd.), and Avalon (PS Analytical Ltd.) software.
Statistical Analyses
The data were analyzed statistically using Genstat (Version 7, VSN International Ltd., Hemel Hempstead, Herts, UK). Performance variates for each growth interval were analyzed by ANOVA with block as a random factor and Se, oil, diet quality, parental age, and their interactions as fixed factors. Four factors were examined: Se supplied in the broiler breeder diets at low or high levels; n-3 FA at low or high levels; progeny feed quality at high or low nutrient density levels, and parental age at 23 or 27 wk of age. All interactions (Se x oil x quality x parental age) were analyzed, although in general, only significant main effects are presented in the tables. All Se and FA variates were analyzed as a split-plot ANOVA, blocked for progeny cages, and treating Se, oil, progeny diet, and parental age as main plot treatments and progeny age as a subplot treatment. Five factors were examined: Se supplied in the broiler breeder diet at low or high levels; n-3 FA in the broiler breeder diet at low or high levels; progeny feed quality at high or low; parental age at 23 or 27 wk of age, and progeny age at 3 levels (0, 7, 14). For all statistical comparisons, where main terms were statistically significant, appropriate pairwise comparisons were made using Fisher’s post hoc least significant difference test, with P 
0.05 taken as significant. Percentage data, such as those of FA and mortality, 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). All Se data were log-transformed prior to analysis. Means and SEM are presented on the original scale. Statements of significance were based on P 0.05, unless otherwise stated. In the tables, the data are presented as the mean ±SEM of each of the main effects in turn, pooled for all other main effects.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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). Chicks from parents fed the Se supplemented diets were 0.5 g heavier at hatch than those fed the low Se diets. In the present study parental age significantly affected all the measured performance parameters (Tables 2–4). The chicks from 27-wk-old breeders where almost 4 g heavier than those from 23-wk-old breeders. At 7 d posthatch, the body mass of chicks hatched from hens fed FO was lower compared with that of chicks hatched from hens fed soya oil, irrespective of parental age. This effect was also evident at 14 d posthatch, when chicks hatched from hens fed FO were 11 g lighter than the chicks that hatched from hens fed soya oil. Selenium supplementation did not affect d 7 or 14 body mass. Adjusting the d 7 and 14 body mass for the difference in body mass at hatching (i.e., using d 0 body mass as a covariant) revealed that the differences in d 7 and 14 body mass attributed to FO were caused by differences in initial body masses. Chicks hatched from eggs laid by the 27-wk-old breeders were heavier than the chicks hatched from eggs laid by the 23-wk-old breeders throughout the 2-wk growing period. At 7 and 14 d post-hatch, the body mass of chicks from 23-wk-old parents was 19.7 and 63.4 g, respectively, lower than that of chicks hatched from 27-wk-old breeders. Chicks that were fed LQ diets had lower body masses at 7 and 14 d posthatch. At 7 d posthatch, chicks fed the LQ diets weighed 8.1 g less than the chicks fed the HQ diets. By 14 d posthatch, the difference in the body masses of chicks fed the LQ and HQ diets was 43.2 g.
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). Supplementation of the broiler breeder diets with FO reduced weight gain during the first week post-hatch, but not the second week, and this was also reflected in cumulative weight gain over the 2 wk. The addition of Se to the breeder diet did not affect the weight gain of the progeny. The weight gain of the progeny was affected by diet quality; chicks fed the LQ diets had lower weight gain throughout the growing period.
Chicks hatched from 27-wk-old breeders had greater feed intake during wk 1 and 2 posthatch, as well as for the overall period (Table 3), compared with chicks hatched from 23-wk-old breeders. The supply of FO or Se in the breeder diet did not affect the feed intake of the progeny. For wk 1 posthatch, chicks consuming the LQ diet had lower feed intake compared with the chicks consuming the HQ diet; however, for wk 2, as well as for the cumulative period, there were no differences in feed intake. The FCR of the progeny was poor and was affected by the quality of the diet and age of the parent bird (Table 3). Chicks hatched from 27-wk-old breeders utilized feed more efficiently compared with chicks hatched from 23-wk-old breeders. This was evident throughout the growing study. There was no main effect of Se or FO addition to the breeder diet on the FCR of the progeny. Chicks consuming HQ diets converted the feed more efficiently to body mass compared with chicks consuming LQ diets.
Broiler breeder age significantly affected the mortality of the progeny (Table 4). Chicks that hatched from eggs laid by the older breeders had lower mortality compared with that of chicks hatched from 23-wk-old broiler breeders. The mortality of chicks hatched from 23-wk-old breeders was 10.6% during the first week of the life, whereas that of chicks hatched from 27-wk-old breeders was about 3 times lower. There was zero mortality in chicks from 27-wk-old breeders at 7 to 14 d, whereas mortality was 5.9% in chicks from 23-wk-old breeders. The overall mortality during the 2-wk growing study was 4-fold higher for chicks hatched from 23-wk-old parents compared with those of 27-wk-old parents. The quality of the progeny diet had no effect on the mortality of the growing chicks; however, the dietary treatments of the parent stock did have a significant effect on the mortality of the progeny. Supplementation of the maternal diet with FO increased the mortality of the chicks during wk 1 of life and consequently the overall mortality during the 2-wk growing period. There was a significant interaction between PUFA supply in the parent diet and parental age in the posthatch changes of cumulative mortality. The inclusion of PUFA in the diet of 23-wk-old breeders resulted in progeny mortality of 22 ±3% overall (0 to 14 d) compared with a mortality of 10 ±2% in chicks from parents fed soya oil only. In contrast, the mortality of chicks from 27-wk-old broilers fed FO was 4.0 ±2% compared with a progeny mortality level of 3.5 ±1% in parents of this age fed diets containing soya oil only. Fish oil did not affect mortality during wk 2 of the growing period, irrespective of the parental age. Supplementation of the maternal diet with Se did not affect the mortality of the progeny.
Selenium Concentration of Chick Tissues
Chicks hatched from breeders fed diets high in Se had higher concentrations of Se in the brain and the liver than chicks hatched from breeders fed diets low in Se. Even after 14 d posthatch, chicks that hatched from parents fed the high Se diets had higher tissue Se concentrations than those hatched from parents fed the diets low in Se, irrespective of tissue type. This observation was evident for both parental ages (Table 5). The Se content of the brain in chicks hatched from hens fed diets high in Se increased by a factor of 1.4 (168 ±4 ng/g) compared with that of chicks hatched from hens fed a diet low in Se (123 ±1 ng/g). Similarly, the Se content of the liver in these chicks increased by a factor of 2.2 (462 ±22 vs. 209 ±5 ng/g). The concentration of Se in the brain of the progeny was consistently lower than in the liver, regardless of parent age, and of the diet of either parents or progeny. Addition of FO to the broiler breeder diet did not affect the concentration of Se in the tissues of the progeny. However, the age and production level of the parent bird affected the concentration of Se in the brain and liver of the progeny. Chicks hatched from 27-wk-old breeders had a lower concentration of Se in the brain and higher concentration of Se in the liver compared with chicks hatched from 23-wk-old breeders. The diet of the progeny did not have an effect on the tissue Se content of the progeny because both diets contained the same level of Se. By 2 wk post-hatch, the Se concentration of the tissues was reduced compared with the concentration of Se in the tissues at d 0. Overall, the reduction of the Se concentration in the brain exhibited a different pattern compared with the reduction of the Se concentration in the liver. The concentration of Se in the liver was reduced during wk 1 post-hatch and then maintained at the same level during wk 2, whereas the Se concentration in the brain continued to decrease throughout the 2-wk period.
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). Chicks hatched from breeders fed diets with FO had an n-6/n-3 ratio of 0.5, whereas chicks hatched from parents fed diets with soya oil had an n-6/n-3 ratio of 1.3. Neither parental age nor Se supplementation of the maternal diet affected the lipid content or the n-6/n-3 ratio in the lipid of the progeny brain. There was a significant interaction between PUFA supply in the parent diet and progeny age (oil x progeny age) in the posthatch changes of the brain lipid content and n-6/n-3 ratio. As the chicks grew, the lipid content of the brain increased and the n-6/n-3 ratio increased. As chicks aged, the amount of DHA as a proportion of total FA in the lipid of the brain also decreased. The concentration of DHA dropped by almost 2% each week, from 17.0 ±0.5% at hatch. At hatching, the brain lipids in chicks from parents fed diets with FO were higher in DHA compared with those from parents fed the soya oil diet. This difference was maintained for up to 14 d posthatch, irrespective of parental age. The concentration of DHA in the brain of chicks originating from parents fed the high Se diets was significantly higher (15.2 ±0.4%) compared with that of chicks hatched from parents fed the low Se diets (14.5 ±0.4%).
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). However, 2 major differences were noted between the 2 tissues. First, the n-6/n-3 ratio in the liver of the chicks was 10 times higher compared with that of the brain, irrespective of the source of the oil that was added to the breeder diet (Tables 6 and 7). Secondly, the lipid content of the liver decreased as the age of the progeny increased, whereas the opposite was true for the brain. For the chicks hatched from Se-supplemented breeders, the concentration of DHA in the liver was significantly higher (4.3%) than that of chicks hatched from the low Se-supplemented breeders (4.0%). This effect of Se was reflected by a lower n-6/n-3 ratio in the chicks hatched from the high Se-supplemented breeders compared with those hatched from the low Se treatments (7.4 ±0.5 vs. 8.8 ±0.6). At hatching, the concentration of DHA in the liver of chicks from parents fed diets rich in PUFA was higher compared with the concentration in the liver of chicks from parents fed the soya oil diet. This difference was maintained up to 14 d posthatch. There was a significant interaction between PUFA supply in the parent diet and progeny age in the posthatch changes of DHA and arachidonic acid [AA, C20:4(n-6)] in the liver and the brain of the chicks (Figures 1 and 2). In both tissues, the decrease of the DHA concentration in chicks hatched from parents fed diets rich in PUFA was accompanied with an increase in the concentration of AA; the birds received a soy oil diet posthatch that was rich in n-6 FA. After 2 wk, the concentration of AA, as grams per 100 g of total FA, in the tissues of progeny hatched from parents fed diets rich in PUFA had almost doubled, whereas in tissues of chicks hatched from breeders fed the diets low in PUFA the increase was not so pronounced.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Changes in the FA profile in the tissues of the progeny due to supplementation of the maternal diet with PUFA observed in the present study were similar to that described previously (Ajuyah et al., 2003). Supplementation of the maternal diet with FO increased the concentration of long chain n-3 PUFA, like DHA, relative to total FA in the yolk (Pappas et al., 2005) and in the tissues of the hatched chick (this study). The concentration of DHA, relative to total FA, in the brain and liver was several times higher than that measured in the hatching egg yolk, even when broiler breeders were fed diets that were low in PUFA. This suggests that the PUFA composition in the brain is not simply a passive reflection of the FA profile of the yolk and may be due to biomagnification of DHA by the yolk sac membrane (Speake et al., 1998b). However, if the total amount of DHA (mg) in the whole yolk and whole brain are compared, then the amount of DHA is far higher in the yolk than in the brain. In fact, only about 5% of the DHA initially present in the yolk is recovered in the brain (Maldjian et al., 1995). However, the physiological function of DHA in brain cell membranes is dependent on the concentration of DHA (as a percentage of the total FA) in brain phospholipids (Salem et al., 2001). The n-6/n-3 ratio in the brain lipid of chicks from breeders fed diets rich in PUFA was similar to that noted in a previous study in which a comparable level of FO (5%) was used in the maternal diet (Ajuyah et al., 2003).
The effects of maternal nutrition in the growing chick in this study persisted for up to 14 d posthatch. Previous studies have indicated similar persistent effects of maternal nutrition on the progeny; however, these studies were conducted in DHA-deficient progeny or by using lard or corn oil in the maternal diet. For example, supplementation of the maternal diet with FO influenced the brain DHA content of the progeny, which were fed a diet deficient in DHA for up to 6 wk posthatch (Ajuyah et al., 2003). In addition, differences in the performance of chicks from breeders fed diets with corn oil or lard persisted up to slaughter age (Peebles et al., 1999a,b). In the present study, chicks that hatched from parents fed diets high in PUFA had higher concentrations of DHA, lower concentrations of AA, and a lower n-6/n-3 ratio in tissue lipids at hatch and for up to 14 d posthatch compared with chicks hatched from parents fed diets low in PUFA, irrespective of progeny diet. The persistence of the effects of maternal nutrition could potentially be exploited to enhance the DHA content of neural tissues in the newly hatched chick. Previous reports indicated that the elongation and desaturation pathways for the conversion of -linolenic acid to DHA do not operate at a sufficient capacity to satisfy the needs of the neural tissues in the early stages of the life of the chick (Anderson and Connor, 1994). Supplementation of the maternal diet with PUFA could increase the concentration of DHA in the tissues of the chick during the first crucial days posthatch and so overcome the apparent shortfall in the chick’s ability to convert -linoleic acid. The neurons of the brain and the photoreceptors of the retina are the major cell types that require high levels of DHA (Neuringer et al., 1988; Lauritzen et al., 2001) and may be reflected in the higher concentration of DHA in brain lipid compared with liver lipid found in chicks in the present study. Animals can synthesize long chain FA, like DHA, from precursor FA. The growing chicks received diets that contained soya oil, and it is possible that the amount of DHA that was synthesized and supplied to the tissues was not sufficient to maintain the high concentration of DHA noted at hatch in the chick tissues. This might explain the posthatch decline in the concentration of DHA in chicks originating from parents fed diets with soya oil or FO. Furthermore, the decrease of DHA in the lipid of the brain and liver of chicks hatched from parents fed diets rich in PUFA was accompanied by an increase in AA, which may indicate an influence of the n-6/n-3 ratio in the maternal (1.89) and progeny diet (12.0) on desaturase activities, as suggested previously (Ajuyah et al., 2003). As the concentration of AA did not alter with age in the chicks originating from soya oil-fed breeders, where both maternal and progeny diets contained similar n-6/n-3 ratio (12.0), this supports the fact that the precursors of AA and DHA compete for the same desaturase enzymes, namely 
6 and 5 (Sprecher, 2000).
The brain exhibits a lower activity of the Se-dependent antioxidative enzyme, glutathione peroxidase (GSH-Px), compared with the liver, which is the tissue that has been shown to have the highest activity of GSH-Px in chickens (Surai, 1999). The combination of high concentrations of oxidation-susceptible PUFA and the lowest antioxidant activities observed means that the chick brain is a tissue that could be very vulnerable to lipid oxidation. Selenium, in the form of selenocysteine, is an integral part of GSH-Px and other selenoproteins. The addition of Se to the diet could, through the action of GSH-Px and other selenoproteins, provide the necessary antioxidant protection required. Although the activity of GSH-Px was not measured in this study, it is possible to infer that it was higher in the tissues of chicks hatched from breeders fed diets high in Se compared with that in tissues of chicks hatched from breeders fed diets low in Se. This hypothesis is supported by the fact that the concentration of DHA in the brain of chicks originating from parents fed the high Se diets was increased by 0.7% compared with that of chicks hatched from parents fed the low Se diets. The same trends in the concentration of DHA in the lipid content of the liver were observed. Additional antioxidant protection provided by increased activity of selenoproteins in the brain could explain the increased content of DHA in the tissues examined.
The concentration of Se provided in the maternal diet not only determined the concentration of Se in the egg (Pappas et al., 2005) but continued to affect the posthatch Se status of the progeny for up to 2 wk. In this study, all the progeny were fed diets with the same concentration of Se, and because feed intake did not differ between treatments, the differences in the Se content of the tissues is due solely to differences in the Se content of the maternal diets. Usually, the Se level fed to breeder hens (0.1 mg·kg–1) is sufficient to prevent Se deficiency conditions in the progeny (Kidd, 2003). This study indicates that the Se levels of the hen diet can increase the Se reserves of the progeny, which could be important in periods of increased demand, such as during hatching or disease challenge. During times of disease challenge, feed intake and thus gut absorption of minerals are depressed; therefore, the reserves present in tissues become increasingly important (Jacques, 2001). Studies in rats revealed that low Se intake by females during pregnancy and lactation reduced the neonatal plasma Se levels and the number of the natural killer cells of the progeny and thus influ-enced the immune system (Dylewski et al., 2002). The same authors reported that adequate Se in the maternal diet was important for the development and function of the cellular and humoral immune system of the neonate. In the present study, the chicks were fed diets with a Se concentration of 0.2 mg/kg. The amount of Se transferred to the tissues might not have been sufficient to maintain the high concentration of Se in the tissues at hatch, which explains the posthatch reduction in Se concentration in the tissues of chicks hatched from breeders fed diets with 0.5 mg of Se/kg
The use of high PUFA concentrations in broiler breeder diets and the subsequent effect of this on the performance of the progeny have been previously described (Hulan et al., 1988; Ajuyah et al., 1993); however, the results are often contradictory. In the present study, the inclusion of FO in breeder hen diets resulted in poor chick performance and a reduction in chick body mass. Most of this effect was caused by a reduction in initial hatching weight of these chicks. Hulan et al. (1988) reported that chicken fed redfish meal or redfish oil had reduced feed consumption and poor performance compared with the control treatment (no FO or fish meal). The authors attributed the adverse effects of FO to poor palatability of the diets rather than to possible oxidation of the FO because the level of vitamin E in the diet was twice the recommended level. Feed intake in the present study was not affected by dietary treatment. Similarly, the supply of full-fat flax seed (high in PUFA) in the chicken diet caused poor growth, irrespective of whether an antioxidant was used (Ajuyah et al., 1993). However, other authors reported that chicks hatched from the breeders fed diets with high PUFA concentrations had high feed intake and feed:gain ratio compared with chicks hatched from breeders fed diets low in PUFA (Zollitsch et al., 1997; López-Ferrer et al., 2001). In the present study, Se addition to the broiler breeder diet did not affect any other performance parameter apart from body mass at hatch. Previously, Se supplementation of broiler diets improved FCR as a result of lower feed intake, while maintaining the same weight gain (Choct et al., 2004).
As anticipated, the chickens fed a diet of poorer nutritional quality (lower protein and energy) had lower body weight gain, higher FCR, and lower body mass at 7 and 14 d posthatch than chicks fed the HQ diets. However, it was anticipated that consumption of the LQ diet would have caused the chicks a certain amount of nutritional stress and that the concentrations of Se in the tissues of these chicks would be somewhat depleted to meet this demand. In this context, one might have expected the progeny that had hatched from breeders fed the high Se diets and fed the LQ diet to perform better than the chicks hatched from breeders fed the low Se diets and fed the LQ diets, but this was not the case. The nutritional stress caused by the LQ diets might not have been severe enough to induce such differences.
Broiler breeder age and stage of production had a sig-nificant effect on hatching chick body mass and the subsequent posthatch performance of the progeny. Chick body mass increased with increasing parent age and egg mass as described previously (Shanawany, 1984; Bruzual et al., 2000; Braun et al., 2002b). Chicks hatched from eggs laid by 27-wk-old parents had higher feed intake, body weight gain and body mass and lower FCR than the chicks hatched from eggs laid by 23-wk-old parents. The growth rate of ducklings from 24-wk-old duck breeders was slower than that of ducklings from 31- or 47-wk-old breeders (Braun et al., 2002b). The positive correlation that exists between hatching egg weight and initial posthatch growth in chickens (Wilson, 1991) and turkeys (Applegate, 2002) was confirmed in the present study.
Mortality was lower in chicks from 27-wk-old hens compared with chicks hatched from 23-wk-old breeders, as has been previously reported (Wilson, 1991). Although the mechanism underlying these differences is uncertain, it is postulated that maternal age affects several factors, the combination of which may correspond to the increased mortality noted in chicks from young hens. Factors that change with maternal age include, but are not limited to, egg weight (Shanawany, 1987), the FA profile of yolk lipid, and the uptake of yolk lipids by the embryo. Broiler breeders at 36 wk of age lay eggs with reduced concentrations of DHA compared with the concentration in eggs laid by 58-wk-old hens (Scheideler et al., 1998). The ability of embryos from 25-wk-old broiler breeders to mobilize the stored lipids of the yolk via the yolk sac membrane was reduced compared with embryos from 41-wk-old hens (Noble et al., 1986). The embryo, therefore, might have a reduced access to its major energy source and the essential nutrients that the yolk lipid contains. A combination of the aforementioned factors may explain the increase in mortality of chicks from hens fed a diet supplemented with FO observed in the present study. In addition, mortality was twice as high in wk 1 compared with wk 2, reflecting the switch from dependence on yolk sac resources to the diet.
The present work has demonstrated that the effects of PUFA and organo-Se compounds supplied in the maternal diet can persist for at least 2 wk posthatch and possibly beyond that, thereby increasing the Se reserves of the progeny. An increase in the Se reserves of the progeny could be important in periods of increased demand for antioxidants, such as during disease challenge. Although the inclusion of PUFA in the breeder diet had no benefits on chick performance, the status of DHA, an indispensable nutrient for good vision and brain function, was enhanced. In addition, Se supplied in the maternal diet can protect the concentration of DHA in the tissues of the progeny.
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ACKNOWLEDGMENTS |
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Received for publication December 22, 2005. Accepted for publication April 29, 2006.
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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), DHA-SO is an open square (
), AA-FO is solid circle (•), and AA-SO is an open circle (
). Data are means ±SEM.