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DL
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Vitamin E and Selenium
« Thread started on: Sep 22nd, 2007, 05:11am » |
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please note that this is a new thread and I will be adding to it extensively in the coming weeks (the added links will not show up as "new" posts ) Please note when reading through the following information that recent studies have concluded that vitaminE and Selenium are interdependent on each other (older studies/research often have not taken this into account)-DL
http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/206924.htm
The 3 main disorders seen in chicks deficient in vitamin E are encephalomalacia, exudative diathesis, and muscular dystrophy. The occurrence of these conditions depends on various dietary and environmental factors.
Encephalomalacia is seen in commercial flocks if diets are low in vitamin E, an antioxidant is either omitted or not present in sufficient quantities, or the diet contains a reasonably high level of an unstable, unsaturated fat. For exudative diathesis to occur, the diet must be deficient in both vitamin E and selenium. Signs of muscular dystrophy are rare in chicks, as the diet must be deficient in both sulfur amino acids and vitamin E. Because the sulfur amino acids are necessary for growth, a deficiency severe enough to induce muscular dystrophy is unlikely to occur under commercial conditions. Signs of exudative diathesis and muscular dystrophy can be reversed in chicks by supplementing the diet with liberal amounts of vitamin E, assuming the deficiency is not too advanced. Encephalomalacia may or may not respond to vitamin E supplementation, depending on the extent of the damage to the cerebellum.
The classical sign of encephalomalacia is ataxia, which results from hemorrhage and edema within the molecular and granular layers of the cerebellum, with pyknosis and eventual disappearance of the Purkinje cells and separation of the molecular and granular layers of the cerebellar folia. Due to its inherently low level of vitamin E, the cerebellum is particularly susceptible to lipid peroxidation. In prevention of encephalomalacia, vitamin E functions as a biologic antioxidant. The quantitative need for vitamin E for this function depends on the amount of linoleic acid and polyunsaturated fatty acids in the diet. Over prolonged periods, antioxidants will prevent encephalomalacia in chicks when added to diets with very low levels of vitamin E, or in chicks fed vitamin E-depleted purified diets. Chicks hatched from breeders that are given additional dietary vitamin E are also less susceptible to lipid peroxidation in the brain. The fact that antioxidants can help prevent encephalomalacia but fail to prevent exudative diathesis or muscular dystrophy in chicks, strongly suggests that vitamin E is acting as an antioxidant. Exudative diathesis results in a severe edema caused by a marked increase in capillary permeability. Electrophoretic patterns of the blood show a decrease in albumin levels, whereas exudative fluids contained a protein pattern similar to that of normal blood plasma.
A vitamin E deficiency accompanied by a sulfur amino acid deficiency results in a severe muscular dystrophy in chicks by ~4 wk of age. This condition is characterized by degeneration of the muscle fibers, usually in the breast but sometimes also in the leg muscles. Histologic examination shows Zenker’s degeneration, with perivascular infiltration and marked accumulation of infiltrated eosinophils, lymphocytes, and histocytes. Accumulation of these cells in dystrophic tissue results in an increase in lysosomal enzymes, the function of which appears to be the breakdown and removal of the products of dystrophic degeneration. Initial studies involving the effects of dietary vitamin E on muscular dystrophy showed that the addition of selenium at 1-5 mg/kg diet reduced the incidence of muscular dystrophy in chicks receiving a vitamin E-deficient diet that was low in methionine and cysteine, but did not completely prevent the disease. However, selenium was completely effective in preventing muscular dystrophy in chicks when the diet contained a low level of vitamin E, which by itself had no effect on the disease.
Studies on the interrelationships between antioxidants, linoleic acid, selenium, and sulfur amino acids have brought some order to the previous confusion about the role of vitamin E in chick nutrition. It is now apparent that selenium and vitamin E play supportive roles in several processes, one of which involves cysteine metabolism and its role in the prevention of muscular dystrophy in the chicken. Glutathione peroxidase is soluble and is therefore located in the aqueous portions of the cell, while vitamin E is located mainly in the hydrophobic environments of membranes and in lipid storage cells. The overlapping manner in which vitamin E and selenium function in the cellular antioxidant system suggest that they spare one another in the prevention of deficiency signs. "
http://www.avianmedicine.net/articles/vitamin-e.doc
doc on vit E
http://ohioline.osu.edu/sc167/sc167_05.html
(a few excerpts)
"....Researchers have found that selenium counteracts the toxicity of other elements such as silver, cadmium and mercury, but it is unlikely that these would play any role in practical poultry nutrition. A greater possibility was the presence of higher concentrations of copper and zinc that would interfere with normal metabolism. Both copper and zinc are used as dietary supplements in feed manufacturing. Broiler rations commonly contain copper supplements providing 120 to 240 ppm in addition to the 5 to 8 ppm included in the trace mineral mix. These levels have been used for years, because they improve performance and are believed to protect against fungal and perhaps other diseases.............Copper-selenium interaction studies showed that copper level influenced the requirement of chicks for selenium (Jensen, 1975b). Adding 800 or 1,600 ppm copper to a diet containing .2 ppm selenium caused high mortality and a high incidence of exudative diathesis and muscular dystrophy. Raising the selenium to .5 ppm prevented the mortality and the pathological conditions. Adding 2,000 ppm or more of zinc also caused high mortality, exudative diathesis and muscular dystrophy in chicks fed a similar diet. Raising the selenium level also prevented these effects.............
Involvement of Selenium in Poultry Diseases
In 1973, I joined the Poultry Science Department at The University of Georgia. A parasitologist on the faculty said he frequently observed a high incidence of greenish, gelatinous edema over the breasts in experimental birds exposed to coccidiosis. Coccidiosis is a major disease in chickens. The edema suggested an inadequate level of dietary selenium. We conducted experiments in which we inoculated chicks with a mixture of five coccidial species at two weeks of age. The chicks received a practical diet with or without selenium and/or vitamin E (Jensen et al., 1978). Mortality in chicks fed the unsupplemented diet reached levels as high as 68%, while those given selenium or vitamin E had much lower mortality.
Many studies have shown that selenium and vitamin E play a role in enhancing the immunity of animals. We studied the effect of these nutrients on the development of immunity to Eimeria tenella in young chicks. The chicks, fed diets with and without .25 ppm selenium or 100 IU vitamin E, were immunized at two weeks of age, then challenged with a high dose of E. tenella at about four weeks. Diet did not influence body weight at time of challenge, but the weight gain six days post-challenge was significantly greater in those fed the supplemented diets (Colnago et al., 1984).
During the conduct of the coccidial immunity experiments pens of chicks had to be kept in two different houses. At three weeks of age the chicks in only one house contracted Malabsorption Syndrome. This disease, also called Pale Bird Syndrome, occurs worldwide in broiler flocks. The etiology of this disease is still not determined, but it appears to be caused by a combination of viral and bacterial agents. Because the chicks were fed diets with and/or without selenium and vitamin E, the effect of these nutrients on the severity of the disease could be observed (Colnago et al., 1983). Thirty-four percent of the chicks fed the basal died, while selenium and vitamin E reduced it to a normal level. The combination of the two nutrients also significantly improved body weight gain...........................
....Selenium and Vitamin E Deficiency Diseases in Poultry
Deficiency diseases in chicks involving inadequate vitamin E or selenium include encephalomalacia, exudative diathesis, nutritional muscular dystrophy and nutritional pancreatic atrophy. Only vitamin E or some synthetic antioxidants prevent the first disease. Either selenium or vitamin E prevents exudative diathesis. To produce muscular dystrophy, the diet must be marginal in cystine. Vitamin E will prevent it, but selenium is only partially effective. Thompson and Scott (1969) found that pancreatic atrophy resulted from a specific deficiency of selenium and that vitamin E (100 IU/kg) could not prevent it. Later studies by Whitacre and Combs (1983), however, showed that very high levels of vitamin E or synthetic antioxidants could prevent the disease.
A vitamin-selenium deficiency in turkey poults differs from that in chicks. The major sign is muscular dystrophy, particularly of the gizzard and heart, but also of the breast muscle. In contrast to chicks, adding high levels of sulfur-containing amino acids has no influence on the myopathy (Walter and Jensen, 1963). Muscular dystrophy in turkeys is caused primarily by a selenium deficiency with vitamin E modifying the amount of selenium needed to prevent the disease.................."
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| « Last Edit: Jul 18th, 2009, 04:41am by DL » |
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DL
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Re: Vitamin E and Selenium
« Reply #1 on: Oct 3rd, 2007, 09:00am » |
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http://www.ansci.cornell.edu/poultry/ppjul00.pdf
CHALLENGE: THE PERCEPTIONS ON SELENITE
(Cornell Univ.)
".....The net result has been the emergence of selenomethionine as a feed supplement, not just as an alternative to inorganic selenium sources, but as a preferred source of selenium. Whether it acts through sparing effect on vitamin E or through its ability to reduce broiler breeder mortality and improve
broiler efficiency, it is clear that selenomethionine will be the preferred source of selenium in the future."
http://compepid.tuskegee.edu/syllabi/pathobiology/pathology/specpath/chapter2.html
"2.8.2 ENCEPHALOMALACIA AND MYELOMALACIA:
Malacia refers to softening and the term is used to indicate necrosis of tissue in the CNS. When myelin sheath is primarily or selectively injured to leave the axon naked by intact, the term demyelination should be used. Actually, malacia, to some degree, is associated with most injuries to the CNS (encephalitis, trauma, anoxia, etc.). Malacia or softening of the gray matter is known as poliomalacia and softening of the white matter is known as leukomalacia......
.....2.8.2.3 AVIAN ENCEPHALOMALACIA:Chicks fed a diet deficient in vitamin E may exhibit one or more of three classical deficiency disorders:
(1) encephalomalacia,
(2) exudative diathesis,
(3) nutritional muscular dystrophy.
Various dietary supplements, unrelated to the vitamin E content of the diet, can prevent any one of the diseases without affecting the course of the other two (synthetic antioxidants can prevent encephalomalacia; ....selenium can prevent exudative diathesis; cystine can prevent nutritional muscular dystrophy).
Encephalomalacia occurs with diets borderline in vitamin E that also contain polyunsaturated fats (cod-liver oil, soybean oil, etc.) in the process of undergoing oxidative rancidity. The disease is characterized by sudden prostration with the legs outstretched, toes flexed, and the head retracted. In early stages, the gait is uncoordinated. Lesions are found in the cerebellum and sometimes in the cerebrum. Softening is prominent and necrotic reddish or brownish areas may be observed with the naked eyes. Microscopically, the lesions are consistent with those of malacia. Exudative diathesis is a frequent occurrence on corn or soybean meal diets when these are grown on selenium deficient soil.
Nutritional muscular dystrophy is found when the diet is deficient in both vitamin E and sulfur-containing amino acids....."
http://www.pjbs.org/ijps/fin696.pdf
Selenium Sources Affect Protein Concentration, Thioredoxin Reductase Activityand Selected Production Parameters in Reovirus Infected Broiler Chickens
http://lib.bioinfo.pl/pmid:17952730
Br Poult Sci. 2007 Oct ;48 (5):580-93 17952730 (P,S,G,E,B) Dietary vitamin E (alpha-tocopherol acetate) and selenium supplementation from different sources: performance, ascites-related variables and antioxidant status in broilers reared at low and optimum temperatures
"....1. This study compared the effect of dietary supplementation with organic or inorganic selenium (Se) sources plus control amounts or large amounts of vitamin E (alpha-tocopherol acetate) in broilers raised at control (20 to 24 degrees C) or low (14.5 to 16.8 degrees C) temperatures after 2 weeks of age. 2. The following dietary treatments were used from one day old. Diet 1, the control diet, comprised a commercial diet containing 0.15 mg/kg inorganic Se and 50 mg vitamin E/kg feed. Diet 2 was the same as diet 1, supplemented with 0.15 mg/kg inorganic Se. Diet 3 was the same as diet 2 but was supplemented with 200 mg/kg vitamin E. Diet 4 was the same as diet 1, but inorganic Se was replaced with 0.30 mg/kg organic Se. Diet 5 was the same as diet 4, supplemented with 200 mg/kg vitamin E. 3. Low temperature reduced the growth rate of broilers; however, at 6 weeks, there were no differences in the body weights of birds fed on organic Se supplemented diets housed at low or control temperature. The feed conversion ratio was significantly affected by low temperature but not by diet. The heterophil/lymphocyte ratio was higher in chicks after one week in the cold, indicating mild stress. Blood triiodothyronine levels were significantly higher in birds after 1 and 4 weeks in the cold but thyroxin was not affected. 4. Organic Se supplementation increased relative lung weight at the control temperature, which might lead to greater respiratory capacity. Relative spleen weight significantly decreased in broilers fed diets supplemented with inorganic Se under cold conditions, a possible indication of chronic oxidative stress. 5. At the low temperature, supplementation with organic Se alone, or with inorganic Se and vitamin E increased glutathione peroxidase (GSHPx) activity and glutathione (GSH) concentration in the liver of broilers, which may indicate increased activity of birds' antioxidant defence against suboptimal environments. ...."
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DL
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Re: Vitamin E and Selenium
« Reply #2 on: Nov 10th, 2008, 06:54am » |
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http://www.lib.ncsu.edu/theses/available/etd-06072004-082938/unrestricted/etd.pdf
(an extensive , excellent review of selenium)
"....In a study in which Se was administered to growing chickens, Se concentrations were found to be dependent on the amount of vitamin E available. The majority of the accumulation of Se was in the feathers (Leibetseder and Leskova, 1973). Selenium concentrations were highest in the kidney and retina, followed by the spleen, liver, bone and plasma. Chickens deficient in vitamin E had a significant decrease in the amount of Se retained in the feathers, blood, and cerebellum, but an increase in the concentration in the liver and breast muscle (Leibetseder and Leskova, 1973). Another study showed similar results......
......Se-deficiency in poultry, especially when combined with a vitamin E deficiency, can be responsible for a range of avian diseases including exudative diathesis (Bartholomew et al., 1998), nutritional encephalomalacia (Century and Hurwitt, 1964; Combs and Hady, 1991), and nutritional pancreatic atrophy (NPA) (Cantor et al., 1975; Thompson and Scott, 1969). NPA is the only disease that is caused by Se-deficiency alone (Combs, 1994). Se-deficiency in chickens is associated with impaired immunocompetence, reduced egg production, and increased embryonic mortality (Combs and Combs, 1984). In a study done by Combs and Scott (1974), birds were fed a low Se diet and peroxidized fat. This resulted in a significant decrease in the hatchability of eggs, which was restored by Se and vitamin E supplementation. Se-deficiency in poultry affects fertility and hatchability. Lathshaw and Osman (1974) reported low fertility and hatchability when birds were fed a basal (low Se) diet, but this reproductive disorder could be corrected partly by vitamin E supplementation and completely by Se-supplementation. Eggs from hens fed a very low level of Se were more likely to be infertile (12.6%), more likely to have high embryo mortality (29%) and lower rate of hatchability of fertile eggs (15%). Mean values for the control group for infertility, embryo mortality, and hatchability were 4.1, 2.9, and 9.1%, respectively (Latshaw et al., 1977). Hatching weights of chicks from hens supplemented with 0.05 26and 0.1 ppm of Se were significantly heavier than those of hens with no supplemental Se. Exudative diathesis (ED) in hatchlings from hens with no Se supplementation was also elevated (Hassan et al., 1990). ED is a common problem in chickens deficient in Se and vitamin E. ED is attributed to increased capillary permeability due to endothelial cell failure in skeletal muscle (Combs and Scott, 1974) and reduced levels of blood proteins (Kristiansen, 1973). The signs of ED arises from leakage of body fluids through the capillaries and from small hemorrhages in the muscle tissues (Hassan et al., 1990) and can occur at any age but most frequently in young chicks or turkey poults (Whitehead and Portsmouth, 1989). Hassan et al. (1990) studied ED in chicks from laying hens fed a Se and vitamin E- deficient diets. ED was observed at hatching whereas signs of ED were not present in the chicks from Se and vitamin E supplemented hens indicating that signs of ED can develop during the development of embryos from Se- and vitamin E-deficient dams. ED has been associated with low levels of muscle Se, liver GSH-px, and an increase in liver non-Se-dependent GSH-px (Hassan et al., 1990). Bartholomew et al. (1998) hypothesized that ED may be an inflammatory response associated with a Se/vitamin E deficiency. Pro-inflammatory cytokines, recruited because of a lack of antioxidant enzymes, might be responsible for the fluid accumulation and hemorrhaging. Supplementing the diet with Se rather than vitamin E is more effective in preventing the occurrence of ED. Vitamin E supplementation at 15 ppm was not enough to prevent ED while levels as low as 0.15 ppm of Se was sufficient (Hassan et al., 1990). Therefore, ED is considered to be a Se-deficiency syndrome in chickens (Machlin et al., 1962). .....
.... In chickens, a low Se diet increased the amount of spermatozoa with bent midpieces to 18.7%, while diets supplemented with either sodium selenite or SeMet decreased the amount of deformed midpieces to 6.2% and 0.7%, respectively (Edens, 2002). These studies have shown that adequate Se is required to maintain sperm membrane integrity, motility, and fertilizing capability. The combination of both vitamin E and Se further improves semen quality. ....
.....Selenosis or Se toxicity in any species, can be classified in two categories depending on the amount of Se ingested and the duration of exposure (Kim and Mahan, 2001). Acute selenosis is a result of a high dietary intake (>20mg/kg) of Se for a short period of time (Miller and Williams, 1940). Signs of acute selenosis are respiratory distress, ataxia, diarrhea, and even death (Mahan and Moxon, 1984). Chronic selenosis is a result of a dietary intake of 5 to 20 mg/kg over a long period of time (Goehring et al., 1984). .....
....The relationship between the immune system and modern day poultry performance is complex. The general opinion is that poultry have a decreased immune system functions due to an increase in selection pressures for increased growth characteristics in a confined environment. In fact, the decreased immune system functions are probably due to nutrient requirements that are no longer being met by the
modern day diet. A proper source of Se supplementation in current poultry diets may be
one factor that can enhance the immune system of poultry. This concept has been demonstrated in many animal studies in which organic Se in Sel-Plex® has been compared with inorganic sodium selenite. In the current study, organic selenium in Sel-Plex® was shown to enhance the immune system while there was a negative impact of sodium selenite. Additionally, Sel-Plex® has been shown to be safe at levels as high as
15 ppm whereas sodium selenite fed birds showed signs of toxicity as low as 1.2 ppm....."
http://www.engormix.com/comparative_metabolic_and_immune_e_articles_121_AVG.htm
"....In most countries the natural selenium content of grain and forages, which consists mainly of the selenoamino acids selenomethionine and selenocysteine in plant proteins, is only 0.03–0.12 mg/kg with values more commonly at the lower end of this range. Intake of such feeds can result in serious selenium deficiency and health problems, especially in highly productive animals. For this reason, feedstuffs are routinely supplemented with various selenium sources at 0.2-0.3 mg Se/kg of dry matter. ....Our results unequivocally confirmed the more efficient utilization of the organic form of selenium in chickens as reflected by its higher levels in tissues, particularly in muscle. The most striking finding in birds given 0.2 mg/kg Se organic selenium was the fact that muscle selenium over the entire experiment was twice that of birds given 0.2 mg/kg Se from selenite. Another noteworthy result was that muscle selenium of those given 0.2 mg/kg Se from selenite did not differ from that of chickens given the unsupplemented basal diet. Moreover, muscle selenium level in 7 week-old birds given inorganic selenium fell to half that at hatch (from 11.8±1.3 to 5.5±0.2 µmol/kg, P<0.001). This means that selenite is unable to supply selenium in a form that allows tissue deposition.
When selenium is supplied in organic form, muscle tissue becomes the most significant storage deposit of selenium in a form of selenomethionine. The reason is that muscle mass represents about 52–56% of body weight. The uptake of selenomethionine by muscle proteins is very important from the point of view of increased transfer of selenium from the dam to eggs and embryos; which is an important determinant of subsequent immunocompetence and health of young birds. ....."
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| « Last Edit: Nov 10th, 2008, 07:18am by DL » |
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DL
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Re: Vitamin E and Selenium
« Reply #3 on: Nov 10th, 2008, 08:04am » |
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http://ps.fass.org/cgi/content/abstract/85/9/1610
Maternal Organo-Selenium Compounds and Polyunsaturated Fatty Acids Affect Progeny Performance and Levels of Selenium and Docosahexaenoic Acid in the Chick Tissues
(Poult Sci 2006. 85:1610-1620)
"...At hatch, and for up to 14 d posthatch, chicks from hens fed diets high in PUFA had higher concentrations of docosahexaenoic acid (DHA) in the brain and liver compared with chicks hatched from hens fed diets low in PUFA. The DHA content of the tissues of chicks from breeders fed diets supplemented with Se was higher than that in chicks from breeders fed unsupplemented diets. Even after 14 d of being fed a diet with identical levels of Se, chicks hatched from parents fed diets high in Se had higher tissue Se concentrations than those hatched from parents fed diets low in Se. Supplementation of the maternal diet of chicks with organo-Se appears to enhance the DHA concentration of the chick brain, which may improve brain function..."
http://lib.bioinfo.pl/pmid:18062833
J Helminthol. 2007 Dec ;81 (4):399-408 18062833 (P,S,G,E,B) Effect of selenium and Ascaridia galli infection on antioxidant biomarkers in broiler chickens: a mathematical model for parasite reduction and host growth.
"....The activity of selenium-dependent glutathione peroxidase (GPX), liver concentration of vitamin E, and plasma and liver selenium levels were used for estimation of the antioxidant status of broiler chickens infected with Ascaridia galli. These biomarkers were recorded in an experiment covering 70 days p.i. At the same time the establishment rate of A. galli in chicken intestines, gain in the host body weight and chicken survival were studied. Broiler chickens (Cobb hybrids) were infected with 1450 embryonated A. galli eggs and treated with Sel-plex. A mathematical model was applied to determine the rate of nematode reduction and the relative rate of gain of host body weight, which are essential kinetic parameters of parasite-host interaction. The activity of GPX increased with both elevated selenium and reduced infection levels. The concentrations of selenium and vitamin E, and the GPX activity in the infected chickens demonstrated a similar pattern of change with time after day 30 p.i. The supplementation of the broilers with dietary selenium in the form of Sel-plex improved their antioxidant status. Increases by 29% in vitamin E concentration, 15% in GPX activity, and 22% in liver selenium concentration, respectively, were recorded in the infected and treated, compared to infected and untreated broilers...."
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DL
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Re: Vitamin E and Selenium
« Reply #4 on: Nov 10th, 2008, 09:10am » |
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http://www.ncbi.nlm.nih.gov/pubmed/10890223?ordinalpos=14&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
Effect of selenium and vitamin E content of the maternal diet on the antioxidant system of the yolk and the developing chick.
Br Poult Sci. 2000 May;41(2):235-43
"...1. The effects of selenium and vitamin E supplementation of the maternal diet on their transfer to the egg yolk and tissues of the newly hatched chick and on the development of the antioxidant system in the chick liver in early postnatal life were investigated. 2. One hundred Cobb broiler breeder hens were divided into 10 equal groups and housed in pens at 25 weeks of age. Each hen received 1 of the treatment diets which included 0.2 or 0.4 mg/kg selenium, 40, 100, 200 mg/kg vitamin E or their combination. After 6 weeks, the hens were artificially inseminated once per week. From week 8, eggs were collected and placed in an incubator. After hatching, chicks from each group were reared (under standard commercial conditions) to 10 d of age. The chicks were fed on a standard starter commercial broiler diet. At the time of hatching, and at 5 and 10 days old, 4 chicks from each group were sacrificed and blood, liver and brain were collected for the subsequent biochemical analyses. 3. The inclusion of organic selenium or vitamin E in the commercial diet significantly increased their concentration in the egg and in the liver of 1-d-old chicks obtained from the eggs enriched with these substances. A positive effect of such dietary supplementation was seen at d 5 and d 10 of postnatal development. 4. There was a positive effect of selenium supplementation of the maternal diet on glutathione concentration in the liver of 1-d-old and 5-d-old chicks. A combination of a dietary selenium supplementation with high vitamin E doses further increased glutathione concentration in the liver. Dietary selenium supplementation significantly increased selenium-dependent glutathione peroxidase (Se-GSH-Px) activity in the liver of the 1-d-old and 5-d-old chicks and decreased liver susceptibility to peroxidation. 6. It is concluded that the nutritional status of the laying hen determines the efficiency of the antioxidant system throughout embryonic and early postnatal development of the offspring....."
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