Clinico-Pathologic Findings in Young Pigs Fed Different Levels of Selenium,Vitamin E and Antioxidant

A randomized, blocked 23 factorial experiment was conducted with 48 young pigs. The treatment factors were: 2 levels of selenium (55 and 115 µg/kg), 2 levels of vitamin E (3 and 53 mg/kg) and 2 levels of the antioxidant feed additive Ethoxyquin (0 and 150 mg/kg). All pigs were kept in single pens and fed ad libitum throughout the experimental period of 9 weeks, i.e. from 3 to 12 weeks of age. Plasma, heart, liver and muscle Se levels as well as whole blood glutathione peroxidase activity (EC 1.11.1.9 GSH-Px) were significantly higher in pigs given a dietary supplement of Se than in pigs given no supplement of Se (P ≤ 0.001). The Se-supplemented pigs showed a tendency to lower mean serum transaminase activity (ASAT and ALAT) than unsupplemented pigs, but the influence was significant (P ≤ 0.05) only for the ALAT activity. Blood vit. E levels were higher for pigs receiving a supplement of vit. E than for unsupplemented pigs (P ≤ 0.001), and so was the resistance of red blood cells against lipid peroxidation (ELP), as expressed by lower ELP values. There were no effects of Ethoxyquin supplementation on the biochemical variables included in the study. The histological examination of heart muscle showed that the score for changes was negatively influenced by both Se and vit. E supplement (P ≤ 0.001) and to some extent also by Ethoxyquin supplement (P ≤ 0.05). The histological picture of m. long dorsi was influenced only by the vit. E supplement (P ≤ 0.01). No histological changes were found in the liver in this study. There were inverse relationships between whole blood GSH-Px defluorescence time and blood Se, and between ELP and whole blood vit. E (P ≤ 0.001).     

Effect of Dietary Fat Quality and Vitamin E on the Antioxidant Potential of Pigs

A randomized blocked factorial experiment was conducted with 90 young pigs. From 4 to 11 weeks of age the pigs were kept in individual pens and fed a selenium supplemented basal diet consisting mostly of propionic acid treated barley, soybean meal and dried skim milk, and containing < 0.5 mg vitamin E per kg. The treatment factors during this period were 3 dietary levels of added vitamin E (nil, 10 and 30 mg/kg) and a 6 % supplement of fresh or oxidized fat (2/3 lard and 1/3 herring oil). From 11 weeks of age until slaughter at 90 kg the pigs received the vitamin E supplements but no fat or dried skim milk. The basal diet for this later experimental period was based on untreated dry barley. Blood samples collected during the period of investigation were examined for vitamin E and for resistance against erythrocyte lipid peroxidation (ELP) in order to evaluate the antioxidant status. Analysis of variance and Student’s t-test on least squares means showed the ELP to be influenced independently by the vitamin E supplement and, during the fat feeding period, by the quality of the fat supplement, with the highest peroxidation resistance (low ELP) in the groups fed fresh fat and a high level of vitamin E. Blood vitamin E level was only influenced — positively — by the vitamin E supplement although variations in the feed vitamin E level below 10–15 mg vitamin E per kg did not result in corresponding variations in measurable blood vitamin E concentrations. In the same low range of vitamin E in the feed there was a statistically significant difference in ELP values between the different vitamin E treatment groups. No clinical manifestations of selenium-vitamin E deficiency were observed in the pigs. The ELP and the plasma vitamin E levels observed would seem to suggest that a total of 15 mg vitamin E per kg barley-based feed will not always be sufficient for growing pigs.     

Selenium and Glutathione Peroxidase Levels in Lambs Receiving Feed Supplemented with Sodium Selenite or Selenomethionine

Twenty-one 6 months old female lambs were divided into 7 groups and fed a basal diet containing 0.13 mg Se/kg. The basal diet was further supplemented with 0, 0.1, 0.5 or 1.0 mg Se/kg either as sodium selenite or as selenomethionine, and was fed for 10 weeks. Both feed additives produced an increase in the selenium concentration in the tissues analysed. Significant correlations were found between the concentrations of selenomethionine or sodium selenite added to the feed and the subsequent tissue levels. However, the selenium levels seemed to plateau at approximately 0.5 mg Se/kg of supplemented sodium selenite. The total glutathione peroxidase (GSH-Px) activity of the tissues increased when the selenium supplementation increased from 0 to 0.1 mg/kg for both selenium compounds. With further increase in selenium supplementation the GSH-Px activity in the tissues plateaued except in the blood where the activity continued to rise with increasing selenomethionine supplementation. The selenium dependent GSH-Px activity in the liver rose with increasing selenomethionine supplementation, but approached a plateau when 0.1 mg Se/kg as sodium selenite was added to the feed. The selenium concentration in whole blood responded more rapidly to the selenium supplementation than did GSH-Px activity. The experiment indicates that the optimal selenium concentration in the feed is considerably higher than 0.1 mg Se/kg, and that selenium levels of 1.0 mg/kg in the feed do not result in any risk for the animals or the consumers of the products.     

Effect of Dietary and Injectable Vitamin E on the Antioxidant Status of Pigs

An experiment concerning 6 different vitamin E treatments was conducted with 30 young pigs. From 4 to 15 weeks of age the pigs were kept in individual pens and fed a selenium supplemented basal diet consisting mostly of propionic acid treated barley and soybean meal, and containing 4.4 mg vitamin E per kg. The treatments were periods with or without vitamin E supplement (20 mg/kg) or a vitamin E injection (200 mg). Blood samples collected during the period of investigation were examined for vitamin E and for resistance against erythrocyte lipid peroxidation (ELP) in order to evaluate the antioxidant status. Analysis of variance showed a litter effect on ELP values at all the weekly investigations and a treatment effect from two weeks after the experiment had started. Also the blood vitamin E level was litter dependent and influenced by treatment. Paired comparisons by Student’s t-test showed a delay of 1 to 2 weeks in the effect on ELP of a dietary vitamin E supplement. In contrast, both ELP and vitamin E changed very rapidly (hours) after vitamin E injections. Independently of the vitamin E treatments there was a rise in ELP within the first 2 or 3 weeks after weaning; this was taken as an index of a reduced antioxidant status during that period.     

Effects of dietary selenium and vitamin E concentrations on phospholipid hydroperoxide glutathione peroxidase expression in reproductive tissues of pubertal maturing male rats

Phospholipid hydroperoxide glutathione peroxidase (PHGPX) is the second intracellular selenium (Se)-dependent glutathione peroxidase (GSH-Px) identified in mammals. Our objectives were to determine the effect of dietary vitamin E and Se levels on PHGPX activity expression in testis, epididymis, and seminal vesicles of pubertal maturing rats, and the relationship of PHGPX expression with testicular development and sperm quality. Forty Sprague-Dawley male weanling rats (21-d old), were initially fed for 3 wk a torula yeast basal diet (containing 0.05 mg Se/kg) supplemented with marginal levels of Se (0.1 mg/kg as Na₂SeO₃) and vitamin E (25 IU/kg as all-rac-α-tocopheryl acetate). Then, rats were fed the basal diets supplemented with 0 or 0.2 mg Se/kg and 0 or 100 IU vitamin E/kg diet during the 3-wk period of pubertal maturing. Compared with the Se-supplemented rats, those fed the Se-deficient diets retained 31, 88, 67, and 50% of Se-dependent GSH-Px activities in liver, testis, epididymis, and seminal vesicles, respectively. Testes and seminal vesicles had substantially higher (5-to 20-fold) PHGPX activity than liver. Dietary Se deficiency did not affect PHGPX activities in the reproductive tissues, but reduced PHGPX activity in liver by 28% (P < 0.0001). Dietary vitamin E supplementation did not affect PHGPX activity in liver, whereas it raised PHGPX activity in seminal vesicles by 43% (P < 0.005). Neither dietary vitamin E nor Se levels affected body weight gains, reproductive organ weights, or sperm counts and morphology. In conclusion, expression of PHGPX activity in testis and seminal vesicles was high and regulated by dietary Se and vitamin E differently from that in liver.     

The influence of dietary selenium and vitamin E on glutathione peroxidase and glutathione in the rat

The effect of dietary selenium (Se) and vitamin E supplementation on tissue reduced glutathione (GSH) and glutathione peroxidase activity has been studied in the rat. Increasing Se intake by 0.4 ppm gave significantly higher enzyme levels in all tissues studied, an effect not influenced by vitamin E intake. Further increasing Se to 4 ppm gave higher enzyme levels in red blood cells only, while in liver was there was a significant decrease in enzyme activity probably reflecting Se hepatotoxicity. In the absence of Se supplements increasing dietary vitamin E to 100 mg/kg diet significantly increased enzyme activity but this effect was modified by simultaneous Se supplementation.Se intake had no effect on GSH levels. Rats on high vitamin E intake 500 mg/kg had a significantly higher tissue GSH level. Dietary Se had a sparing effect on vitamin E, rats supplemented with Se having significantly raised plasma vitamin E levels.These results confirm the role of selenium in glutathione peroxidase and also show that vitamin E influences the activity of the enzyme.     

Effect of vitamin E and selenium supplementation of cockerel diets on glutathione peroxidase activity and lipid peroxidation susceptibility in sperm, testes, and liver

The phospholipids of avian spermatozoa are characterized by high proportions of arachidonic (20:4n-6) and docosatetraenoic (22:4n-6) fatty acids and are therefore sensitive to lipid peroxidation. α-Tocopherol and glutathione peroxidase [GSH-Px] are believed to be the primary components of the antioxidant system of the spermatozoa. The present study evaluates the effect of vitamin E and vitamin E plus Se supplementation of the cockerel diet on GSH-Px activity, vitamin E accumulation, and lipid peroxidation in the spermatozoa, testes, and liver. At the beginning of the experiment 75 Rhode Island Red cockerels were divided into five groups, kept in individual cages, and fed a wheat-barley-based ration balanced in all nutrients. Supplements fed to the different groups were as follows: vitamin E, 0, 20, 200, 20, and 200 mg/kg to groups 1–5, respectively, with groups 4 and 5 also receiving 0. 3 mg Se/kg. The vitamin E supplementation produced increased levels of α-tocopherol in semen, testes, and liver. The inclusion of the Se into the cock diet had a significant (P < 0.01) stimulating effect on GSH-Px activity in seminal plasma, spermatozoa, testes, and liver. The increased vitamin E concentration in the spermatozoa was associated with a reduction in their susceptibility to lipid peroxidation. Similarly, the increased GSH-Px activity provided enhanced protection against lipid peroxidation.     

Effects of Dietary Form of Selenium on Its Distribution in Eggs

The objective of this experiment was to investigate the selenium distribution in eggs from hens fed diets supplemented with Se from sodium selenite (SS) or selenium-enriched yeast (SY). One-day-old female chickens of Hy-Line Brown breed were randomly divided into four groups according to dietary treatments and, for the subsequent 9?months, were fed diets which differed only in the form or amount of Se supplemented. During the whole experiment, group 1 (control) was fed basal diet (BD) with only background Se level of 0.13?mg/kg dry matter (DM). Diets for groups 2 and 3 consisted of BD supplemented with an Se dose of 0.4?mg/kg DM either in the form of SS or SY, respectively. Group 4 was fed BD supplemented with 0.9?mg Se/kg DM from SY. After 9?months of dietary treatments, the Se levels in egg yolk and albumen from hens fed unsupplemented diet were almost identical whereas eggs from hens given diet supplemented with SS showed significantly higher Se deposition in yolk than in albumen (P?相似文献   

Parameters of dietary selenium and vitamin E deficiency in growing rabbits.

4 x 5 growing female rabbits (New Zealand White) with an initial live weight of 610 +/- 62 g were fed a torula yeast based semisynthetic diet low in selenium (<0.03 mg/kg diet) and containing <2 mg alpha-tocopherol per kg (group I). Group II received a vitamin E supplementation of 150 mg alpha-tocopherylacetate per kg diet, whereas for group III 0.40 mg Se as Na-selenite and for group IV both supplements were added. Selenium status and parameters of tissue damage were analyzed after 10 weeks on experiment (live weight 2,355 +/- 145 g). Selenium depletion of the Se deficient rabbits (groups I and II) was indicated by a significantly lower plasma Se content (group I: 38.3 +/- 6.23 microg Se/mL plasma, group II: 42.6 +/- 9.77, group III: 149 +/- 33.4, group IV: 126 +/- 6.45) and a significantly lower liver Se content (group I: 89.4 +/- 18.2 microg/kg fresh matter, group II: 111 +/- 26.2) as compared to the Se supplemented groups III (983 +/- 204) and IV (926 +/- 73.9). After 5 weeks on the experimental diets differences in the development of plasma glutathione peroxidase were observed. As compared to the initial status group (45.2 +/- 4.50) pGPx activity in mU/mg protein was decreased in group I (19.1 +/- 7.08), remained almost stable in the vitamin E supplemented group II (46.3 +/- 11.2) whereas an elevated enzyme activity was measured in the Se supplemented groups III (62.4 +/- 23.9) and IV (106 +/- 19.9). In the rabbit organs investigated 10 weeks of Se deficiency caused a significant loss of Se dependent cellular glutathione peroxidase activity (GPx1) of 94% (liver), 80% (kidney), 50% (heart muscle) and 60% (musculus longissimus dorsi) in comparison to Se supplemented control animals. Damage of cellular lipids and proteins in the liver was due to either Se or vitamin E deficiency. However damage was most severe under conditions of a combined Se and vitamin E deficiency. It can be concluded that the activity of plasma glutathione peroxidase is a sensitive indicator of Se deficiency in rabbits. The loss of GPx1 activity indicates the selenium depletion in various rabbit organs. Both selenium and vitamin E are essential and highly efficient antioxidants which protect rabbits against lipid and protein oxidation.     

Effects of Selenium Administration on Erythrocyte and Blood Plasma Glutathione Peroxidase Activity in Goats

The activity of glutathione peroxidase (GSH-Px, E.G. 1.11.1.9.) was determined in heparinized whole blood, blood plasma and washed erythrocytes from goats before and up to 4 weeks after the administration of selenium (0.4 mg/10 kg BW) and vitamin E (20 mg/10 kg BW) or only vit. E (20 mg/10 kg BW). It was found that Se administration caused a significant increase in enzyme activity in whole blood and washed erythrocytes first detected 2 weeks after the intramuscular injection of Se. No changes were observed in plasma from the treated animals. Minor and insignificant changes were seen in the vit. E treated control animals. It is concluded that GSH-Px activity in blood plasma or serum is of no value as a short-term indicator of the selenium status of goats but whole blood is a good indicator of the long-term status.     

The Influence of Supplements of Selenite,Selenate and Selenium Yeast on the Selenium Status of Dairy Heifers

The aim of the study was to define possible differences between selenite, selenate and selenium yeast on various aspects of selenium status in growing cattle. Twenty-four Swedish Red and White dairy heifers were fed no supplementary selenium for 6 months. The basic diet contained 0.026 mg selenium/kg feed dry matter (DM). After the depletion period the animals were divided into 4 groups; group I–III received 2 mg additional selenium daily as sodium selenite, sodium selenate, and a selenium yeast product, respectively. Group IV, the control group, received no additional selenium. The total dietary selenium content for groups I–III during the supplementation period was 0.25 mg/kg DM. After the depletion period the mean concentration of selenium in blood (640 nmol/l) and plasma (299 nmol/l) and the activity of GSH-Px in erythrocytes (610 µkat/l) were marginal, but after 3 months of supplementation they were adequate in all 3 groups. The concentration of selenium in blood and plasma was significantly higher in group III than in groups I and II, but there was no significant difference between groups I and II. The activity of GSH-Px in erythrocytes did not differ between any of the supplemented groups. The animals in the control group had significantly lower concentrations of selenium in blood and plasma and lower activities of GSH-Px in erythrocytes than those in the supplemented groups. The activity of GSH-Px in platelets was also increased by the increased selenium intake. There was no difference in the concentration of triiodothyronine (T3) between any of the groups, but the concentration of thyroxine (T4) was significantly higher in the unsupplemented control group.     

Effect of selenium and a-tocopherol supplementation on postpartum reproductive function of dairy heifers at pasture

The objective of this study was to investigate the effects of selenium (Se) and alpha-tocopherol supplementation on uterine involution and ovarian function in dairy heifers fed a prepartum diet containing low concentrations of Se and alpha-tocopherol. Twenty-four pregnant Friesian heifers were randomly allocated to one of four experimental groups in a 2 x 2 design balanced for age and body weight. Prepartum treatments consisted of supplementation with either 2 intraruminal Se pellets or 3600 mg of alpha-tocopherol p.o. 4 times per wk, or both. Control animals received no supplementation. For 8 wk before calving, the heifers were fed exclusively on pasture hay which contained less than 10 microg/kg of Se and 19 mg/kg of alpha-tocopherol. After calving, the heifers grazed perennial ryegrass and white clover pasture. Concentrations of Se and alpha-tocopherol in serum for the prepartum heifers of the control group were 10 ng/ml and 1.3 microg/ml, respectively, indicating deficiencies of these nutrients. Treatment with Se and alpha-tocopherol increased prepartum serum concentrations of Se and alpha-tocopherol to 74 ng/ml and 5 microg/ml, respectively (P < 0.001). However, treatment with Se, alpha-tocopherol, or both, failed to enhance uterine involution, hasten resumption of postpartum ovarian activity or reduce the incidence of clinical postpartum abnormalities. These findings suggest that postpartum reproductive dysfunction is not a primary feature of moderate Se or vitamin E deficiency of cattle at pasture.     

Effects of inadequate vitamin E and/or selenium nutrition on the release of arachidonic acid metabolites in rat alveolar macrophages

Effects of vitamin E and/or selenium (Se) deficiency on the secretion of arachidonic acid metabolites by zymosan-stimulated pulmonary alveolar macrophages (AM) were examined using cells from male Long-Evans hooded rats fed torula-yeast based diets with or without the supplementation of vitamin E (150 IU/kg) or Se (0.5 mg/kg). Alveolar macrophages obtained by lavage were purified by adherence and cultured for 4 h in Hank's balanced salt solution containing bovine serum albumin (0.1%) and zymosan (300 micrograms/ml). The arachidonic acid metabolites present in the culture supernatant were measured by radioimmunoassay. Altered vitamin E and Se nutrition had no effect on the number of cells or cell types recovered from the pulmonary airways. Alveolar macrophages derived from animals fed on diets deficient in vitamin E or Se or both nutrients secreted higher levels of prostaglandin E2 and thromboxane B2. Levels of both 5-hydroxyeicosatetraenoic acid and leukotriene B4 were significantly increased only in the group fed the diet adequate in Se but deficient in vitamin E. Our data suggest that vitamin E and Se might play an important role to control the levels of several physiologically and pathologically important arachidonic acid metabolites.     

Effects of inadequate vitamin E and/or selenium nutrition on the release of arachidonic acid metabolites in rat alveolar macrophages

Effects of vitamin E and/or selenium (Se) deficiency on the secretion of arachidonic acid metabolites by zymosan-stimulated pulmonary alveolar macrophages (AM) were examined using cells from male Long-Evans hooded rats fed torula-yeast based diets with or without the supplementation of vitamin E (150 IU/kg) or Se (0.5 mg/kg). Alveolar macrophages obtained by lavage were purified by adherence and cultured for 4 h in Hankś balanced salt solution containing bovine serum albumin (0.1%) and zymosan (300 μg/ml). The arachidonic acid metabolites present in the culture supernatant were measured by radioimmunoassay. Altered vitamin E and Se nutrition had no effect on the number of cells or cell types recovered from the pulmonary airways. Alveolar macrophages derived from animals fed on diets deficient in vitamin E or Se or both nutrients secreted higher levels of prostaglandins E₂ and thromboxane B₂. Levels of both 5-hydroxyeicosatetraenoic acid and leukotriene B₄ were significantly increased only in the group fed the diet adequate in Se but deficient in vitamin E. Our data suggest that vitamin E and Se might play an important role to control the levels of several physiologically and pathologically important arachidonic acid metabolites.     

Effects of dietary vitamin E and selenium on antioxidative defense mechanisms in the liver of rats treated with high doses of glucocorticoid

The aim of this work was to determine the effects of dietary intake vitamin E and selenium (Se) on lipid peroxidation as thiobarbituric acid reactive substances (TBARS) and on the antioxidative defense mechanisms in the liver of rats treated with high doses of prednisolone. Two hundred fifty adult male Wistar rats were randomly divided into five groups. The rats were fed a normal diet, but groups 3, 4, and 5 received a daily supplement in their drinking water of 20 mg vitamin E, 0.3 mg Se, and a combination of vitamin E and Se, respectively, for 30 d. For 3 d subsequently, the control group (group 1) was treated with a placebo, and the remaining four groups were injected intramuscularly with 100 mg/kg body weight (BW) prednisolone. After the last administration of prednisolone, 10 rats from each group were killed at 4, 8, 12, 24, and 48 h and the activities of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) enzymes and the levels of glutathione (GSH) and TBARS in their livers were measured. GSH-Px, SOD, and CAT enzyme activities and GSH levels in prednisolone-treatment group (group 2) began to decrease gradually at 4 h, falling respectively to 38%, 55%, and 40% of the control levels by 24 h, and recovering to the control levels at 48 h. In contrast, prednisolone administration caused an increase in the hepatic TBARS, reaching up to four times the levels of the control at 24 h. However, supplementation with vitamin E and Se had a preventive effect on the elevation of the hepatic TBARS and improved the diminished activities of the antioxidative enzymes and the levels of GSH. Therefore, the present study demonstrates the effectiveness of vitamin E and Se in reducing hepatic damage in glucocorticoid-treated rats and suggests that reductions in increased TBARS as a result of prednisolone may be an important factor in the action of vitamin E and Se.     

The potential effects of antioxidant feed additives in mitigating the adverse effects of corn naturally contaminated with <Emphasis Type="Italic">Fusarium</Emphasis> mycotoxins on antioxidant systems in the intestinal mucosa,plasma, and liver in weaned pigs

Seventy-two piglets (6.0 kg BW) were randomly distributed within six different dietary treatments to evaluate the effect of deoxynivalenol (DON) and the potential of four antioxidant feed additives in mitigating the adverse effects of DON on growth performances and oxidative status. Dietary treatments were as follows: control diet 0.8 mg/kg DON; contaminated diet (DON-contaminated diet) 3.1 mg/kg DON; and four contaminated diets, each supplemented with a different antioxidant feed additive, DON + vitamins, DON + organic selenium (Se)/glutathione (GSH), DON + quercetin, and DON + COMB (vitamins + Se/GSH + quercetin from the other treatments). Although DON was the main mycotoxin in the contaminated diet, this diet also contained 1.8 mg/kg of zearalenone (ZEN). The “mycotoxin” effects therefore included the combined effect of these two mycotoxins, DON, and ZEN. The DON-ZEN ingestion did not affect growth performances, average daily gain (ADG), average daily feed intake (ADFI), and feed efficiency (G:F ratio), but partially induced oxidative stress in weaned pigs as shown by increased malondialdehyde (MDA) content in the plasma and superoxide dismutase (SOD) activity in liver (P?<?0.05). However, no change in the activity of other antioxidant enzymes or GSH concentrations was observed in plasma and liver of piglets fed the DON-contaminated diet (P?>?0.05). Supplementation with individual antioxidant feed additive had a limited effect in weaned pigs fed DON-ZEN-contaminated diets. Combination of antioxidants (vitamins A, C, and E, quercetin, and organic Se/GSH) reduced plasma and liver MDA content and SOD activity in liver (P?<?0.05) of piglets fed DON-ZEN-contaminated diets. Furthermore, this combination also reduced MDA content in the ileum (P?<?0.05), although activity of glutathione peroxidases (GPx), SOD or catalase (CAT) in the ileum was not affected by DON-ZEN contamination or antioxidant supplements. In conclusion, DON-ZEN contamination induced oxidative stress in weaned pigs and combination of antioxidant feed additives restored partially the oxidative status. Further studies will be necessary to assess whether the effects of antioxidant feed additives on oxidative status are specific when feed is contaminated with DON-ZEN.     

Comparison of selenium level and glutathione peroxidase activity in tissues of vitamin B6-deficient rats fed sodium selenite or DL-selenomethionine

The effect of vitamin B₆ on the levels of tissue selenium (Se) and glutathione peroxidase (GSH-Px) was studied. Male Wistar 4-week-old rats were fed a vitamin B₆-Se-deficient basal diet for 2 weeks, then divided into 10 groups of five or six rats and fed their respective diets for 4 weeks. The experimental design was a 2×2×2 factorial with two levels of vitamin B₆, two forms of Se, and two levels of Se, plus two extra groups (vitamin B₆-supplemented and deficient without Se). Vitamin B₆ was 0 and 250 μg pyridoxine-HCl/100 g of diet; Se forms were Na₂SeO₃ and DL-selenomethionine; Se levels were 0.5 and 5.0 mg Se/kg of diet. Regardless of form or level of Se, vitamin B₆-deficient rats had lower body weights and organ weights than vitamin B₆-supplemented rats. At 5.0 mg Se/kg of diet, Na₂SeO₃ caused a further depression. Vitamin B₆ deficiency resulted in a higher Se level and GSH-Px activity in plasma of rats fed selenomethionine. However, Se content an GSH-Px activity in erythrocytes were significantly elevated in vitamin B₆-supplemented rats compared with vitamin B₆-deficient rats. Se levels in muscle and heart were significantly lower in vitamin B₆-deficient groups fed Na₂SeO₃ than in vitamin B₆-supplemented groups. Vitamin B₆-deficient rats fed selenomethionine had higher Se levels in muscle, heart, spleen, liver, and kidneys than vitamin B₆-supplemented rats. Activity of GSH-Px in muscle, heart, and spleen was significantly lower in vitamin B₆-deficient groups than in vitamin B₆-supplemented groups, regardless of form of Se. A significant decrease of GSH-Px in liver was observed in vitamin B₆-deficient rats fed selenomethionine compared with vitamin B₆-supplemented rats, whereas no significant decrease was observed in those fed Na₂SeO₃. These results suggest that vitamin B₆ is involved in the distribution and transportation of Se in body and the metabolism of selenomethionine in liver.     

Barium Selenate as a Slow-Release Selenium Preparation to Pigs

Pregnant sows were injected subcutaneously (s.c.) or intramuscularly (i.m.) with a barium selenate suspension (0.5–1.0 mg Se/kg body weight (b.w.)) and together with control animals fed a commercial diet. No response to the injection was seen either in blood selenium levels or in glutathione peroxidase (GSH-Px) activity in the sows. There was, however, a significant difference in these parameters between piglets born from treated dams and control animals. This status was maintained during the nursing period. In another experiment pigs (20 kg b.w.) on a Se-deficient diet were injected s.c. and i.m. with barium selenate (2.5 mg Se/kg b.w.). The treated groups maintained their blood levels of selenium and GSH-Px activity, although the selenium values in the group treated intramuscularly started to decline after 4 weeks. Organ samples from both groups were equal with regard to selenium at the time of slaughter while the control group showed a rapid decline both in blood selenium levels and GHS-Px activity.     

Vitamin E and selenium supplementation to alleviate cold-stress-associated deterioration in egg quality and egg Yolk mineral concentrations of Japanese quails

The effects of vitamin E (dl-α-tocopheryl acetate) and selenium (Se; Na₂-SeO₃) on egg production, egg quality, and mineral content of egg yolk in Japanese quails reared under a low ambient temperature (6°C) were evaluated. Birds (n=300; 7 wk old) were randomly assigned to 12 treatment groups, 25 birds per group. The birds in a 3×2 factorial design received either three levels of vitamin E (125, 250, and 500 mg/kg diet) or two levels of selenium (0.1 or 0.2 mg/kg diet). After 2 wk on feed, six groups of the birds were maintained at 18°C (thermoneutral temperature [TN]), and the other half were acclimated over 3 d to a decreased environmental temperature of 6°C (cold stress [CS]). The performance, egg quality, and mineral content of egg yolk were not influenced by supplemental vitamin E and selenium in quails not exposed to cold stress (p≥0.09). Two hundred fifty and 500 mg vitamin E/kg diet compared with 125 mg/kg diet and higher dietary selenium inclusions (0.2 vs 0.1 mg/kg) resulted in a better body weight, egg production, and feed efficiency (p=0.01) in quails reared under CS. Similarly, egg weight, egg specific gravity, eggshell thickness, and Haugh unit were positively influenced with vitamin E (p=0.01) and selenium (p≤0.05) supplementation. Egg yolk concentrations of Zn, Fe, and Mn were higher with higher dietary vitamin E (p=0.01) and selenium (p=0.05). There was no interaction detected for parameters measured in the present study (p≥0.3). The results of the present study showed that a combination of 250 or 500 mg vitamin E and 0.2 mg selenium per kilogram of diet provides the greatest effects on performance and egg quality of Japanese quails reared under cold stress and suggest that such a supplementation can be considered as a protective management practice in Japanese quail diets to reduce the detrimental effects of cold stress.     

Alterations in plasma total and high density lipoprotein cholesterol levels in hyperlipidemic rats fed diets with varied content of selenium and vitamin E

The effect of dietary selenium and vitamin E on plasma total (TC) and high density lipoprotein cholesterol (HDLC) was evaluated in 54 Sprague Dawley rats fed cholesterol/cholic acid enriched diets. Diets 1, 2, and 3 had no added selenium (low Se) and 0 (low), 60 (adequate), and 600 (high) mg/kg dL alpha tocopheryl acetate added respectively. Sodium selenite at 0.2 mg/kg (adequate Se) was added to diets 4, 5, and 6 and at 4.0 mg/kg (toxic Se) to diet 7, 8, and 9 with the same pattern of vitamin E added to the diet as described above. TC and HDLC were measured using the Kodak Ectachem system. Rats in the low and adequate Se groups fed high vitamin E had lower TC values than rats fed lower vitamin E levels but differences were not significant. In the toxic Se groups, rats fed high vitamin E had significantly (p<0.05) higher plasma TC values than did lower Vitamin E groups. Rats on the high vitamin E diets with low or adequate Se had significantly (p<0.05) higher mean plasma HDLC values when compared to rats fed low or adequate vitamin E diets. HDLC values for animals on Se toxic diets were significantly (p<0.05) lower in rats fed a low vitamin E diet. In rats fed Se deficient and adequate diets, a high vitamin E intake resulted in a decrease in TC and an increase in HDLC. In Se toxic rats, TC was elevated by a high dietary intake of vitamin E as was HDLC with both values being significantly higher than values found in the vitamin E deficient rats. Vitamin E deficiency resulted in a plasma lipid pattern that has been associated with greater cardiovascular disease risk.