Studies on vitamin E and selenium deficiency in young pigs. III. Effect on kinetics of erythrocyte production and destruction.

The effect of vitamin E and/or selenium deficiency on the kinetics of erythrocyte production and destruction has been investigated in swine. The plasma iron turnover rate, 59Fe incorporation into newly formed red cells as well as the 51Cr apparent red cell half-life, were not found to be significantly affected by either vitamin E deficiency, selenium deficiency or deficiency of both, as compared to replete animals. The results of this study suggest that vitamin E is not a limiting factor for normal erythropoiesis in young growing pigs. Erythropoiesis appeared, however, to be slightly decreased in selenium deficient pigs and will need to be further investigated.     

Studies on vitamin E and selenium deficiency in young pigs. IV. Effect on coagulation system.

An evaluation of the coagulation system has been conducted in vitamin E and/or selenium deficient swine. The partial thromboplastin time, plasma fibrinogen concentration, platelet lipid peroxides, as well as the fibrinogen/fibrin degradation products were not found to be significantly affected by either vitamin E deficiency, selenium deficiency, or deficiency of both. With selenium deficiency, the prothrombin time was shortened (p less than 0.05). The platelet count and platelet turnover were greatly decreased by both vitamin E (p less than 0.001) and selenium deficiency (p less than 0.005). Further-more, the survival of platelets labelled with 75Se-selenomethionine and the per cent isotope incorporated into platelets were reduced (p less than 0.05 and p less than 0.005) in association with vitamin E deficiency, but not with selenium deficiency. These results were interpreted as evidence of a platelet production defect and possibly a platelet function defect in vitamin E deficient animals. Selenium deficiency were also associated with decreased (p less than 0.05) survival of fibrinogen labelled with 75Se-selenomethionine and increased (p less than 0.05) turnover of fibrinogen. From these fibrinogen kinetic findings, it was considered that chronic low grade disseminated intravascular coagulation possibly occurs in selenium deficient animals, probably in relation to the development of hepatosis dietetica or widespread microvascular damage. However, other possibilities such as increased fibrinogenolysis in relation with hepatosis dietetica or an intrinsic fibrinogen defect due to selenium deficiency also need to be taken into consideration and have not been ruled out in the present study.     

Congenital nutritional muscular dystrophy in a beef calf

A 13-hour-old Aberdeen-Angus was involuntarily recumbent since birth. Congenital nutritional muscular dystrophy was suspected based on clinical findings, increased serum creatine kinase, and decreased serum vitamin E and selenium levels. Recovery followed after supportive therapy and parenteral vitamin E and selenium. Reports of this disease in newborn calves are unusual.     

Studies on vitamin E and selenium deficiency in young pigs. II. The hydrogen peroxide hemolysis test and the measure of red cell lipid peroxides as indices of vitamin E and selenium status.

The usefulness of the hydrogen peroxide hemolysis test and the measure of red cell lipid peroxides as indices of vitamin E and selenium deficiency in swine has been evaluated. Results indicated that although the hydrogen peroxide hemolysis test may be of some indication of the vitamin E status, it is not a reliable index of vitamin E deficiency in swine, at least on an individual basis. In contrast, the measure of red cell lipid peroxides can be considered a reliable test for vitamin E deficiency in swine. The hydrogen peroxide hemolysis test and the red cell lipid peroxides were not significantly affected by selenium deficiency.     

Effects of monensin on selenium status and related factors in genetically hypo- and hyperselenemic growing swine.

Monensin is an ionophoretic antibiotic, which selectively transports alkali metal cations across biological membranes. In growing swine, monensin toxicosis causes acute, degenerative cardiac and skeletal myopathy resembling vitamin E-selenium deficiency. Selenium is an essential trace element incorporated in glutathione peroxidase (GSH-Px), an antioxidant enzyme system that protects subcellular membranes. In our study, we examined the effects of monensin on body weight, Se balance, antioxidant status, and serum concentrations of selected minerals in growing pigs that were genetically hypo- or hyperselenemic (hypo-Se and hyper-Se, respectively). Three groups of eight 8-week-old pigs, each comprised of 4 hypo-Se and 4 hyper-Se pigs (76.4 +/- 3.0 and 106.3 +/- 10.3 ng of Se/ml of serum, respectively), were fed standard diets containing 0.1 mg of supplemental Se/kg of body weight, and either 0, 200, or 400 mg of monensin/kg for a 77-day period, followed by a 28-day monensin withdrawal period. On days 0, 7, 28, 56, 70, and 98, all pigs were weighed and blood was collected for determination of serum GSH-Px, creatine phosphokinase, and aspartate transaminase values, as well as serum concentrations of vitamin E, Se, Ca, Cu, Fe, K, Mg, Na, P, and Zn. Significance of main effects of monensin treatment, genetic Se status, and their interactions was tested by Fisher's variance ratio test, followed by conditional comparison of treatment means with a Bonferroni test. Signs of monensin toxicosis were not observed and monensin consumption had no effect on body weight, or serum creatine phosphokinase, aspartate transaminase, or Se values. However, pigs consuming monensin had consistently higher serum GSH-Px activities, possibly because of increased synthesis of this adaptive antioxidant enzyme. Interactions were not found between monensin and genetic Se status. Hyperselenemic pigs were heavier and had higher serum Se and GSH-Px values than hypo-Se pigs. Furthermore, hypo-Se and hyper-Se pigs were hypo- and hypercupremic, respectively, suggesting genetic regulation of copper status. It is likely that pigs with inadequate antioxidant status (hyposelenemia, hypocupremia) are more susceptible to diseases associated with cellular membrane damage, such as vitamin E-Se deficiency disease and monensin toxicosis.     

Vitamin E requirements of laying hens

In 5 experiments with 1,296 laying hybrids at the age of 22-73 weeks producing eggs for consumption a varied supplementation of between 0 and 20 mg vitamin E per kg of a semisynthetic ration was tested. The vitamin E content of the basal ration was less than 1 mg per kg feed. The quotas of selenium and unsaturated fatty acids in the feed were taken into consideration. Vitamin E and Se supplements did not influence, feed intake, laying, performance, feed efficiency/100 g egg development of body weight and mortality. The supplementation of 14% vitamin-E-free sunflower oil caused a significant decrease of the laying performance by 15%. There was no relation between the humoral immune reaction and vitamin E supply. The peroxide value of the abdominal fat and the activities of the creatine phosphokinase, the aspartate and alanine amino transferase in the blood serum were not directionally changed by the vitamin E, Se and oil supplements. There were no significant relations between the vitamin E content of the feed and that of the yolk and the yolk sac of the chicken. A vitamin E requirement of less than 1 mg and a requirement norm, including a safety margin, of 5 mg per kg feed was derived from the results for laying hens for egg production. A supplement of synthetic vitamin E to laying hen feed is thus not necessary.     

Studies on serum selenium and tocopherol in white muscle disease of foal

In order to clarify the cause of white muscle disease (W.M.D.) in foals, tocopherol and selenium concentrations in serum and glutathione peroxidase activities in blood were measured. Examination was made on the samples from horses affected with W.M.D., the foal kept with them in the same stable, the foals kept in the stables without affected foals, and respective mares. The heavy-breed horses in Fukuoka prefecture and Tokachi district were also examined for comparison. Serum tocopherol levels of these foals were normal because after intake of colostrum. Mares of affected foals showed lower tocopherol levels than other examined mares (p less than 0.01). Serum selenium levels of all foals were below 65 ppb, showing deficient levels. The mares of affected foals had lower selenium levels than other mares (p less than 0.01). There was a good correlation between serum selenium concentration and blood glutathione peroxidase activity (r = 0.81). Selenium levels in the liver of affected foals were lower than the foals which succumbed with other diseases. Diet supplied in the stables with affected foals showed low alpha-tocopherol and selenium contents. These findings suggest that W.M.D. in foals is attributed to nutritional muscular dystrophy caused by tocopherol and selenium deficiency of their mares in late gestation period.     

Anemia,myopathy, and pansteatitis in vitamin E-deficient captive marmosets (Callithrix spp.)

Five young adult pet marmosets (Callithrix spp.) were presented with weight loss (5/5); fecal retention (3/5); diarrhea (2/5); impaired locomotion (3/5); anemia (4/4); hypoproteinemia or hypoalbuminemia (3/4); elevations of creatine phosphokinase, lactic dehydrogenase, and alanine aminotransferase (3/4); and renal failure with hypercholesterolemia (2/4). All anemic marmosets had low serum vitamin E levels. The anemia responded to vitamin E and selenium therapy in two marmosets. One of the five marmosets died before presentation, and two others died despite therapy. The two marmosets necropsied had degenerative myopathy, pyogranulomatous pansteatitis, and increased erythrophagocytosis and hemosiderosis. The striated muscle and adipose tissue of both marmosets were negative for coxsackievirus ribonucleic acid by in situ hybridization. These findings suggest that vitamin E deficiency may be involved in the development of anemia, myopathy, and steatitis in callitrichids; however, in some marmosets, underlying diseases such as chronic colitis may have influenced the development of anemia and impaired vitamin E status.     

Clinical and biochemical response in the prevention of nutritional myodystrophy in heifers

Clinical and biochemical responses were studied after taking the measures to prevent nutrition muscular dystrophy in young cattle in the given ecological conditions. Analyzing the biological material (blood, hair, feed, soil), we found the sufficiently high saturation of heifer organisms with the microelement selenium and on the contrary, vitamin E deficiency. Sensitive indicators of the break-down of muscular tissue were the enzymes aspartate aminotransferase (AST), alanine aminotransferase (ALT), and mainly creatinine kinase (CPK): the activities of these enzymes increased significantly after the heifers had been driven to pasture. The stay of animals in the run to get them used to the physical load before going to the pasture was not found to be a sufficient measure to prevent muscular nutrition myodystrophy if the animals had not been administered vitamin E and selenium supplements. Of the one hundred heifers we examined, seven animals began to show the signs of nutrition muscular dystrophy; none of these animals had been administered vitamin E and selenium supplements.     

Studies on serum tocopherol, selenium levels and blood glutathione peroxidase activities in calves with white muscle disease

For the purpose of clarifying the cause of white muscle disease (WMD) in calves, tocopherol and selenium levels and blood glutathione peroxidase (GSH-Px) activity were measured on 10 calves with WMD and nine of their dams. The main clinical symptoms of the 10 calves with WMD were motor disturbances including recumbency and stiffness. Serum enzyme activities (GOT, GPT, CPK, LDH) in calves with WMD increased markedly, and this increase was also observed in some of their dams. Serum tocopherol levels of calves with WMD were low, 70% of which showing deficient levels of less than 70 micrograms/100 ml. Serum selenium levels of all the calves were lower than 35 ppb, indicating a deficiency, and were accompanied by low blood GSH-Px activity. alpha-Tocopherol and selenium concentrations in organs were very low. Dams of calves with WMD showed low serum tocopherol levels, 22% of which indicating deficient levels below 150 micrograms/100 ml. Serum selenium levels in dams showed a marked decrease to under 20 ppb, and also low blood GSH-Px activity. Feedstuffs supplied in the farms to affected calves indicated very low alpha-tocopherol contents (below 3 mg/100g DM) and low selenium concentrations below 50 ppb in DM. It was concluded that WMD in calves was attributable to nutritional muscular dystrophy caused by deficiencies in tocopherol and selenium in feedstuffs supplied to their dams.     

Effects of continuous supplementations of ascorbic acid, aspirin, vitamin E and selenium on some haematological parameters and serum superoxide dismutase level in broiler chickens

1. This study was conducted using male broiler chickens to determine the effects of ascorbic acid, aspirin, ascorbic acid+aspirin, vitamin E+selenium and ascorbic acid+aspirin+vitamin E+selenium supplementations on haematological parameters and serum superoxide dismutase concentration. 2. One hundred and twenty day-old male Hubbunt broiler chicks were randomly divided into 6 experimental groups of 20 chicks each and placed in different pens. Groups 2, 3, 4, 5 and 6 were given a diet supplemented with ascorbic acid, aspirin (in water), ascorbic acid+aspirin, vitamin E+selenium and ascorbic acid+aspirin+vitamin E+selenium, respectively for 45 d while group 1 was given a commercial broiler diet. 3. There was no significant effect of ascorbic acid, aspirin, ascorbic acid+aspirin, vitamin E+selenium supplementations on any of the haematological parameters (red blood cell, haemoglobin, haematocrit, mean corpuscular volume, mean corpuscular haemoglobin concentration, mean corpuscular haemoglobin) in broilers but ascorbic acid+aspirin+vitamin E+selenium supplementation significantly decreased the white blood cell counts. 4. In addition to this, ascorbic acid, aspirin, ascorbic acid+aspirin and ascorbic acid+aspirin+vitamin E+selenium supplementations had no significant effect on the serum superoxide dismutase level, but vitamin E+selenium supplementation increased the serum superoxide dismutase level.     

The selenium and vitamin E status of horses in Prince Edward Island

Serum selenium (Se), vitamin E, and resting thyroid hormone concentrations were measured in 201 horses in Prince Edward Island (PEI). Selenium concentrations were either marginal (0.0053 to 0.1200 ppm) or deficient (< 0.0053 ppm) in 79% of horses based on current reference ranges for Se in serum. Aged and young adult pleasure horses had a higher prevalence of inadequate Se concentrations compared to racehorses and broodmares (82% and 97% versus 45% and 72%, respectively). Overall, 13% of horses had inadequate (< 200 μg/dL) serum vitamin E concentrations; most of these were young pleasure horses. No horses were hypothyroid and, contrary to findings in other species, there was a positive relationship between serum thyroxine and Se concentrations (P < 0.05). We conclude that Se deficiency is widespread in PEI horse populations, especially in pleasure horses, and vitamin E deficiency is more common in young pleasure horses. Micronutrient supplementation practices employed by PEI horse owners appear inadequate to ensure sufficiency.     

Dystrophin‐deficient muscular dystrophy in two lurcher siblings

Two cases of dystrophin‐deficient muscular dystrophy in 16‐week‐old male lurcher siblings are reported. The myopathies were characterised by regurgitation, progressive weakness and muscle wastage. The dogs had generalised weakness in all four limbs, with more pronounced weakness in the pelvic limbs. Reduced withdrawal in all limbs, muscle contracture and lingual hypertrophy were noted. Serum creatine kinase activities were markedly elevated. Electromyographic abnormalities included fibrillation potentials. Histopathological and immunohistochemical staining were consistent with dystrophin‐deficient muscular dystrophy. Clinical improvement was noted in one of the cases with l ‐carnitine supplementation and supportive therapy. Genetic transmission of the disease was postulated as the dogs were siblings.     

维生素E缺乏对鲤骨骼肌损伤的影响

本文旨在探讨VE缺乏对鲤骨骼肌损伤的形态学影响。在半纯合日粮中分别添加0、25、50和100 mg/kg的VE,投喂体重约60 g的鲤鱼20周。结果表明:鲤鱼摄入VE缺乏的饲料后,出现“瘦背症”、脊柱弯曲及以突眼、竖鳞和腹水为特征的渗出性素质样病变。病理剖解见体壁肌肉萎缩,特别是背部两侧肌肉萎缩变薄,其厚度仅为对照组的1/4~1/2,似刀刃状;体侧红肌纤维褪色变白,呈白肌肉外观。组织学变化主要表现为肌营养性不良,骨骼肌变性、坏死,淋巴细胞和单核细胞浸润,大量结缔组织增生,残存的肌纤维萎缩变细。超微结构上表现为骨骼肌细胞核膜间隙增宽,呈锯齿状,并发生局部或广泛性的断裂,核变形,电子密度降低;肌浆内糖原颗粒明显减少,线粒体肿胀,嵴断裂,甚至溶解呈空囊泡状,肌原纤维的横纹模糊不清或完全消失。结论:日粮中0、25和50 mg/kgVE水平会导致鲤出现VE缺乏症,其骨骼肌主要表现为变性、坏死、肌萎缩和炎症细胞浸润的肌营养性不良。     

Effects of vitamin E, age and sex on performance of Japanese quail. 1. Haematological indices and liver function

1. A trial was conducted to examine the effects of dietary vitamin E content, age and sex on haematological indices and liver enzymes of Japanese quails. A total of 800 1-d-old quail chicks were assigned at random into 4 equal groups and fed on starter and layer diets containing 0, 1, 5 or 10 times the NRC recommended supplements of vitamin E. No selenium was added to the basal deficient diets; the other diets were supplied with 0.2 mg selenium/kg diet. 2. The investigation covered the age span of 3 to 12 weeks in female and male birds. Blood samples were collected at 3-week intervals and tested for haematological indices (erythrocyte count; leucocyte count; susceptibility of erythrocytes to haemolysis; haemoglobin concentration (Hb); packed cell volume (PCV); and mean corpuscular volume (MCV)) and liver enzymes (aspartate transaminase, AST, and glutathione peroxidase, GSH-Px). 3. The significant differences between the 4 dietary treatments indicated that as the levels of selenium and/or vitamin E increased, the percentage of erythrocytes haemolysed and AST activity decreased, whereas Hb and GSH-Px concentrations increased. 4. Differences between age groups showed that older quails had higher erythrocyte susceptibility to haemolysis, higher AST levels and but lower erythrocyte count and PCV. 5. Females had lower erythrocyte haemolysis and higher Hb concentrations than males. 6. The interaction between dietary groups and age groups revealed that the differences between age groups were reduced as the level of selenium and/or vitamin E increased, leading to similar group means over the age period of study. 7. In conclusion, NRC recommended supplements of vitamin E (12 and 25 mg/kg diet) were not adequate. Doses equal to, at least, 5 times that recommended were advised to improve GSH-Px (index of antioxidant status) and Hb concentrations.     

Congenital nutritional myodegeneration (white muscle disease) in a red deer (Cervus elaphus) calf

CASE HISTORY A 5-day-old red deer calf was submitted with tachypnoea and dyspnoea, and was reluctant to move.

CLINICAL FINDINGS: Muscular damage was established via elevated creatinine phosphokinase (CPK) activities (5,000 U/L), while concentrations of Se in whole blood were low (24.8 nmol/L). The animal died despite treatment with penicillin-streptomycin and 0.1 mg/kg Se/vitamin E administered by S/C injection.

DIAGNOSIS: Necropsy and histological examination of cardiac and skeletal muscle confirmed the presumptive diagnosis of congenital white muscle disease (WMD). Prophylactic administration of a Se/vitamin E commercial preparation (as above) to another calf born in the same herd one month later was associated with good health and apparently normal growth and development.

CLINICAL RELEVANCE: Congenital WMD due to Se deficiency can be fatal in red deer calves. However, prophylactic administration of Se and vitamin E to neonatal calves may be beneficial for neonatal red deer calves.     

Use of sodium hydroxide treated selenium deficient barley to induce vitamin E and selenium deficiency in yearling cattle

Selenium deficient barley grown in Northern Ireland was treated with sodium hydroxide to deplete it of vitamin E. Housed cattle fed a complete diet based on this treated barley developed nutritional degenerative myopathy, showing that spontaneous myopathy in yearling cattle can be the result of vitamin E and selenium deficiency alone. The diet used is as effective and cheaper than others presently in use for inducing degenerative myopathy.     

Vitamin E, Selenium and Methionine Supplementation of Dystrophogenic Diets for Pigs

Forty-eight weanling S.P.F. Yorshire pigs were used to study the influence of supplemental vitamin E (25 IU per kg of diet) selenium (0.5 ppm in diet) and methionine (0.1% in diet) on the incidence of hepatosis dietetica and mulberry heart disease when fed a torula yeast-corn diet. Vitamin E and/or selenium increased pig survival. Supplemental selenium resulted in increased liver selenium concentrations. No hepatosis dietetica was observed in any of the pigs. The addition of vitamin E and/or selenium at the levels used did not reduce the frequency of myocardial lesions; however, they prevented skeletal muscular dystrophy and exudative diathesis. The myocardial lesions were less severe in supplemented pigs compared with unsupplemented controls.     

Infleuce of dietary levels of vitamin E and selenium on tissue and blood parameters in pigs.

Eighteen barrows approximately three weeks of age were used in a 3 X 3 factorial arrangement to investigate the effect of level of supplemental vitamin E and selenium on tissue and blood parameters. Tissue selenium concentrations increased in a quadratic manner with increased selenium intake with kidney tissue containing considerably greater concentrations than liver, heart or muscle. Supplementation of the diet caused a three-fold increase in serum selenium within the first week with a slight tendency to further increases in subsequent weeks. Serum vitamin E of unsupplemented pigs declined by fifty percent during the experiment, whereas supplemental vitamin E resulted in increased serum vitamin E. There was a considerable viration in percent peroxide hemolysis. Correlation of -0.63 between percent peroxide hemolysis and vitamin E intake and -0.85 between percent peroxide hemolysis and serum vitamin E were observed.