Vitamin E-selenium Deficiency Research Articles

Retrospective review of the pathology of American pikas.

American pikas (Ochotona princeps) are small lagomorphs that live in mountainous talus areas of western North America. Studies on the histopathology of American pikas are limited. We summarize here the clinical histories, and gross and histologic findings of 12 American pikas, including 9 captive (wild-caught) and 3 wild animals. Death was often attributed to stress (transport, handling, anesthesia) with few-to-no premonitory clinical signs. Infection was the cause of death in 2 cases: 1 had bacterial pyogranulomatous dermatitis, cellulitis, and lymphadenitis with sepsis; the other case had oomycete-induced necrotizing colitis. Incidental parasitic infections included sarcocystosis, nematodosis (oxyurids), and ectoparasitism. Most animals with adequate nutritional status had periportal hepatic lipidosis; this finding was absent in all animals with adipose atrophy, and it is possible that periportal hepatic lipidosis is non-pathologic in American pikas. Three cases had myocardial necrosis that was considered the cause of death; the cause of necrosis was not determined, but it may have been caused by stress or vitamin E-selenium deficiency. Esophageal hyperkeratosis was noted in animals with a history of anorexia and negative energy balance; accumulation of esophageal keratin can result from lack of mucosal abrasion by ingesta. Several histologic findings that are likely normal in American pikas include splenic extramedullary hematopoiesis, thymic tissue in adults, and Clostridium sp. in the enteric lumen.

A Summary of New Findings on the Biological Effects of Selenium in Selected Animal Species-A Critical Review.

Selenium is an essential trace element important for many physiological processes, especially for the functions of immune and reproductive systems, metabolism of thyroid hormones, as well as antioxidant defense. Selenium deficiency is usually manifested by an increased incidence of retention of placenta, metritis, mastitis, aborts, lowering fertility and increased susceptibility to infections. In calves, lambs and kids, the selenium deficiency demonstrates by WMD (white muscle disease), in foals and donkey foals, it is associated with incidence of WMD and yellow fat disease, and in pigs it causes VESD (vitamin E/selenium deficiency) syndrome. The prevention of these health disorders can be achieved by an adequate selenium supplementation to the diet. The review summarizes the survey of knowledge on selenium, its biological significance in the organism, the impact of its deficiency in mammalian livestock (comparison of ruminants vs. non-ruminants, herbivore vs. omnivore) and possibilities of its peroral administration. The databases employed were as follows: Web of Science, PubMed, MEDLINE and Google Scholar.

Sudden infant death syndrome and enteric infection

The association of Helicobacter pylori in the stomach, trachea and lungs with the incidence of SIDS, gastric ulcers and cancer may have a counterpart in animals. In field studies of white muscle disease (WMD) and hepatic necrosis in selenium-deficient pigs dying suddenly, veterinarians identified gastric ulcers in 40% of inspected piglets. The lesion was also commonly observed by researchers in experimentally produced vitamin E-selenium deficiency and other researchers suspected that gastric ulcers in swine may be associated with vitamin E-selenium deficiency. Mice preferentially concentrated 75selenium in peritoneal exudative cells (PEC) when 75selenium as selenium selenate was administered by stomach tube to selenium-deficient mice. Selenium concentrated in PECs as glutathione peroxidase (GSHPx). GSHPx-deficient leucocytes in peritoneal exudate failed to kill yeast cells. GSHPx deficiency has also been associated with decreased microbicidal activity of leucocytes in patients with chronic granulomatosis. The selenium-deficient swine were usually growing rapidly in crowded conditions, and, apart from WMD and hepatic necrosis, edema was prominent in the spiral colon, subcutaneous tissues, lungs and submucosa of the stomach. The elevated immunological response in the spleen and lungs of SIDS victims suggests an initial defective microbicidal propensity of the peritoneal exudative cells.

Glutathione Peroxidase Activity and Vitamin E Concentrations in Bearded Dragons, Pogona vitticeps

ABSTRACT Nutritional deficiencies or imbalances are an unfortunate sequela to improper feeding and husbandry of exotic pets. The dietary requirements for many vitamins and minerals have not been established in captive reptiles. Clinical signs of limb paresis and ataxia unresponsive to vitamin D3 or calcium have been observed in bearded dragons, Pogona vitticeps, and some clinicians hypothesize that it may be caused by vitamin E-selenium deficiency. The purposes of this study were 1) to measure plasma vitamin E concentrations and erythrocyte glutathione peroxidase activity in bearded dragons eating different diets, and 2) to determine whether the paresis syndrome recognized in these animals is caused by vitamin E or selenium deficiency. Plasma α-tocopherol concentrations and erythrocyte glutathione peroxidase activity were measured in 34 healthy and one clinically affected captive bearded dragons. Mean concentrations for α-tocopherol (23.23 ± 18.63 μmol/L) and glutathione peroxidase activity (209.02 ± 72.6...

Early muscle injuries in a standard reared stock of sea bass Dicentrarchus labrax, (L.)

An early myopathy affecting the myotomes of a stock of sea bass is described. By electron microscopical examination different degrees of muscle lesions were first detected in recently hatched larvae. Muscle fibres underwent a degenerative process, that according to the gravity of the lesions and age of the fish was sequenced in four stages. Necrotic muscle fibres were abundant in the myotomes of post-larvae (more than 60 days). Although this degenerative myopathy is non-specific, the importance lies in its progressive sequence. Vitamin E-selenium deficiency and uncontrolled peroxidation of the lipid content in the feed is thought to be the cause of the problem. The possible implication of the myopathy in the appearance of a high percentage of lordosis in the same stock of sea bass is discussed.

Creatine kinase in the dog: a review.

In the dog, creatine kinase (CK) is mostly present in the skeletal muscles, myocardium, brain and intestine. The MM isoenzyme predominates in muscles and myocardium. In plasma, reference values depend on the technique used and CK-MB accounts for about 30-45% of total CK activity. Sex has no influence on plasma CK activity, which is higher in young dogs than in adults. Plasma CK is elevated after physical exercise. After its release from the cells, CK reaches the plasma mostly via the lymphatic route and then remains in the plasma compartment. It is rapidly cleared with a half-life of about 2 hours. Muscle diseases are the main source of plasma CK elevations: inherited myopathies, malignant hyperthermia, hypothyroidism, vitamin E-selenium deficiency, prolonged decubitus, intramuscular injections, surgery, etc. Plasma CK is also increased in experimental myocardial infarction, for which the dog is an interesting model, allowing quantification of the damage by measuring the total CK activity released.

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

Summary 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.

Differential Effects of High Dietary Levels of Vitamin A on the Vitamin E-Selenium Nutrition of Young and Adult Chickens

Experiments were conducted to determine the nature of the interaction of high levels of vitamin A and vitamin E-selenium nutrition in the chicken. Results showed that chicks were protected from the vitamin E-selenium deficiency disease exudative diathesis (ED) by a high dietary level of vitamin A (1.0 X 10(6) IU/kg) which moderately depressed growth. A greater concentration (1.5 X 10(6) IU/kg) of vitamin A in the diets of hens fed a low vitamin E diet hastened their depletion of plasma tocopherols and increased plasma glutathione peroxidase (GSH-px) activity. At hatching the progeny of vitamin A-fed hens were severely depleted of plasma tocopherols but had normal plasma GSH-px activities. They showed increased susceptibility to ED when fed selenium-deficient, vitamin E-free diets for 2 weeks. Absorption studies using ligated duodenal loops or oral doses indicated that high-level dietary vitamin A promoted the enteric absorption of selenium but interfered with the absorption of vitamin E. The dual nature of these effects was related to the ED-protective influence of vitamin A when fed to chicks, and the ED-stimulative influence on progeny when vitamin A was fed to dams.

Polychlorinated Biphenyl-Stimulated Selenium Deficiency in the Chick

Experiments were conducted to determine individually the effects of dietary PCBs on the physiologic functions of vitamin E and selenium. Results showed that dietary PCBs did not affect the function of vitamin E in protection of biological membranes. However, PCBs did decrease the biological utilization of dietary selenium as measured by glutathione peroxidase activity in plasma and by the protection of biological membranes from peroxidation. These results indicate that dietary PCBs potentiate vitamin E-selenium deficiency in the chick by interference with the biological utilization of dietary selenium. An hypothesis for the mechanism of this effect is offered.

Effects of Dietary Polychlorinated Biphenyls on Vitamin E and Selenium Nutrition in the Chick

Experiments were conducted to determine the effects of polychlorinated biphenyls (PCBs) on vitamin E-selenium nutrition in the chick. Results showed that 10 p.p.m. Aroclor(R) 1254 in the diets of breeding S.C.W.L. hens increased the susceptibility of progeny to vitamin E-selenium deficiency when those chicks were reared on a diet deficient in vitamin E and supplemented with a marginal level of selenium. Susceptibility to this deficiency, as measured by the incidence of exudative diathesis, was also increased when PCBs were added to chick diets.Dietary PCBs were shown to induce hepatic microsomal benzopyrene hydroxylase and induction of this activity was associated with decreased biological utilization of dietary selenium. PCBs were shown to increase the apparent requirements of the chick for vitamin E and selenium for prevention of exudative diathesis. However, discrimination between effects on vitamin E function and effects on selenium function was not possible in these experiments.

Ultrastructure of Gastrointestinal Smooth Muscle in Ducks with a Vitamin E-Selenium Deficiency

The earliest ultrastructural lesions involving smooth muscle of duck duodenum and gizzard produced by a vitamin E-selenium deficiency were a degereration of sarcoplasmic reticulum and mitochondria. Lysosomes were not observed during these earliest alterations of deficient smooth muscle. Lipid droplets and mineral deposits were present in more severely degernerating smooth muscle that was being infiltrated by heterophils. In areas of necrotic smooth muscle, myoblasts were forming while macrophages, fibroblasts, and an occasional syncytial giant cell contained lipid droplets and surrounded coalesced mineral crystals. Endothelial cells of capillaries and stromal connective tissue were less severely affected with lesions developing after the earliest signs of smooth muscle degeneration. Neuroaxonal degeneration of nonmyelinated nerve fibers was not observed until after most of the smooth muscle had undergone either degeneration or necrosis. A possible explanation for the pathogenesis of the smooth muscle necrosis is discussed in light of the ultrastructural findings.

Alleviating Mortality Associated with a Vitamin E-Selenium Deficiency By Dietary Ascorbic Acid

Adding ascorbic acid to a practical ration deficient in vitamin E and selenium for the growing duck substantially reduced associated mortality. The continued appearance of various myopathies but absence of vascular faults supported implication of a reduced de novo ascorbate synthesis as part of the syndrome. Presumably, alleviation of this induced secondary inadequacy with its more lethal pathology was the primary reason for the lower death rate.

Vitamin E-Selenium Deficiency in the Duck Aggravated by the Use of High-Moisture Corn and Molding Prior to Preservation

A commercial variety of corn harvested in the high-moisture state from a single field was the grain source for growing ducks. Part of this corn was heat-dried to a lower moisture and acted as control, while the remainder was preserved with added propionic acid. Paralleling optimal circumstance, half of the high-moisture grain was treated immediately. To simulate an extreme in poor field management, the remaining wet corn was allowed to mold in a grain cart before acid was added. Whole-grain storage of all treatments ensued for 6 months prior to grinding and dietary incorporation.

Vitamin E-selenium deficiency and its influence on avian malarial infection in the duck.

Vitamin E-selenium deficiency and its influence on avian malarial infection in the duck.

Nutritional hepatic necrosis in beef cattle. "Sawdust liver".

A histologic examination of spontaneous cases of sawdust livers in cattle indicated that the focal liver necrosis was an expression of vitamin E-selenium deficiency. The condition was reproduced in Hereford steers by feeding a diet rich in polyunsaturated fatty acids and poor in protein, vitamin E. and selenium. Lesions also occurred in the kidney, heart, skeletal muscled and pylorus. Addition of dictary protein or injection of selenium partially prevented the condition.Cellular anoxia with formation of hyalinc bodies in the liver and kidney was considered to be the common denominator of the degenerative changes. Due to the relatively mild tissue changes, plasma GOT and OCT determinations were found to be of no diagnostic value.