Blind Staggers Research Articles

The essentiality of selenium for humans, animals, and plants, and the role of selenium in plant metabolism and physiology

AbstractAfter its discovery, selenium was most noted for its harmful effects. Selenium was the first element identified to occur in native vegetation at levels toxic to animals. Poisoning of animals can occur through consumption of plants containing toxic levels of selenium. Livestock consuming excessive amounts of selenized forages are afflicted with “alkali disease” and “blind staggers”. Typical symptoms of these diseases include loss of hair, deformed hooves, blindness, colic, diarrhoea, lethargy, increased heart and respiration rates, and eventually death. On the other hand, selenium deficiency in animal feeds can cause “white muscle disease”, a degenerative disease of the cardiac and skeletal muscles. In this regard, this review paper attempts to summarize the essentiality of selenium for humans, animals, and plants and the role of selenium in plant metabolism and physiology.

Effects of selenium on animal health

Selenium is an essential trace element in the diet of humans and domesticated animals. It is a component of more than 30 selenoproteins, which play a significant role in the body. Selenoproteins protect cells from damage inflicted by free radicals, the cause of many chronic diseases. They also participate in the metabolism of thyroid hormones, control reproductive functions and exert neuroprotective effects. In addition to its anti-proliferative and anti-inflammatory properties, selenium stimulates the immune system. The role of selenium is aided by vitamin E and sulfur-containing amino acids. Selenium deficiency contributes to pathological changes in farm animals, which incur large financial losses each year. Low selenium levels can lead to the development of nutritional muscular dystrophy, also known as white muscle disease, in lambs, kids, foals, calves and poultry from birth to 3 months of age. Selenium deficiency may also cause exudative diathesis in poultry as well as dietary necrotic liver degeneration and mulberry heart disease in pigs. Parturition problems resulting from reduced tension of the muscular layer of the uterus, postparturient paraplegia, placental retention and purulent inflammations of the uterine lining are also attributed to low selenium levels. Selenium deficiency contributes to the formation of ovarian cysts and increased embryonic mortality in the first 3-4 weeks after insemination. Selenium and vitamin E facilitate neutrophil migration to the mammary gland, and they enhance the bactericidal effects of neutrophils, thus shortening and alleviating the symptoms of clinical mastitis. Selenium poisoning is rarely encountered, and it most often results from an overdose of selenium supplements. The most common forms of selenosis are chronic selenosis, referred to as alkali disease, and acute selenosis, popularly known as blind staggers.

Bimodal actions of selenium essential for antioxidant and toxic pro-oxidant activities: The selenium paradox (Review)

Selenium is an essential biological trace element. Adult daily intake of selenium should be approximately 100 µg per day. This compound has a two-sided effect depending on its concentration. A selenium-deficient diet is associated with various endemic diseases, including cardiomuscular malfunctions, osteoarthritis, cancer and viral infections that lead to premature death. These defects are prevented when dietary intake of selenium is adequate. The preventive biological effect of selenium is considered to be due to the antioxidant function of selenoproteins with a selenocysteine in the active site of the catalytic domain. Antioxidant selenoproteins maintain the intracellular redox status and, as a result, normal physiological processes in the cell. Conversely, an overdose of selenium generates oxygen radicals and leads to apoptotic cell death by inducing oxidation and cross-linking of protein thiol groups essential for cell survival. A lower redox state caused by selenium may be implicated in toxic diseases, such as alkali disease and blind staggers. Collectively, selenium seems to have both harmful and beneficial attributes. The aim of this review is to summarize the various biological functions of selenium and to illustrate its opposite roles as a pro-oxidant and an antioxidant.

Enfermidades associadas à intoxicação por selênio em animais

Por meio de revisão da literatura pertinente foram coligidos e são apresentados os principais dados relativos à intoxicação por selênio em animais domésticos. Foram abordados e discutidos os aspectos epidemiológicos, clínicos, anátomo e histopatológicos e patogenéticos atribuídos a Alkali Disease, Blind Staggers, intoxicação aguda e poliomielomalácia simétrica focal dos suínos. O trabalho tem como objetivo esclarecer pontos obscuros relativos à intoxicação por selênio, bem como alertar para os riscos que a suplementação com esse elemento pode representar.

Aspectos clínico-patológicos da intoxicação experimental por selenito de sódio em eqüinos

Dadas as controvérsias sobre a intoxicação por selênio, foram realizados nove experimentos com a administração de selenito de sódio, por via intramuscular, em eqüinos, com o intuito de estudar e melhor fundamentar os aspectos clínico-patológicos e toxicológicos sobre esse tema. Conseguiram-se produzir quadros com evoluções superaguda, aguda, subaguda e crônica; alguns sinais clínicos de origem nervosa observados nos quadros agudos foram similares aos descritos para "blind staggers"; a despeito disto, o carácter conflitante e duvidoso das descrições sobre essa pretensa entidade historicamente descrita, não permite uma comparação mais exata. O quadro crônico, por outro lado, configurou claramente a primeira reprodução de "alkali disease", por via parenteral, em eqüinos. Estabeleceu-se 1,49 mg/kg de selenito de sódio como a dose única letal para essa espécie. Descrevem-se diversos achados clínico-patológicos relativos aos sistemas cardiovascular e nervoso, antes não mencionados na literatura relativa aos eqüinos intoxicados por selênio. Entre eles, destacam-se, clinicamente, sopro e arritmia cardíacos, desdobramento de bulhas e convulsão. À necropsia, um animal apresentou nítido achatamento das circunvoluções cerebrais e, em relação à histopatologia, lise e necrose de neurônios do córtex, edema de astrócitos, bem como ativação endotelial e gliose. Em relação à patogênese, postula-se que as alterações degenerativo-necróticas observadas no sistema nervoso central, devam-se ao edema, por sua vez conseqüente ao aumento da permeabilidade vascular, determinada pelo selenito de sódio.

Selenosis.

Despite more than six decades of research, some aspects of the natural history of selenosis remain confused in modern texts. The primary targets of acute Se toxicity in food animal species are the cardiovascular, gastrointestinal, and possibly hematopoietic systems. Swine may develop neurologic lesions; however, the signs of poliomyelomalacia are quite distinct from those described as "blind staggers" by early workers. The most characteristic signs of chronic selenosis are hair and hoof loss; however, other, less specific, damage to the immune system and reproduction are economically more important. Given the numerous interactions of chronic Se with other dietary factors, it is very important to examine the whole environment when dealing with a potential selenosis case.

Increase in dopamine metabolites in murine striatum after oral exposure to inorganic but not organic form of selenium.

Selenium (Se) is an essential as well as a toxic trace element. Se intoxication has been reported in both livestock and humans. The central nervous system is sensitive to Se poisoning; exposure to Se causes blind staggers in cattle, poliomyelomalacia in pigs, and nervous system disorders in humans. Differences in neurotoxicity between inorganic and organic Se have been demonstrated. In this study, groups of five male BALB/c mice each were administered sodium selenite or selenomethionine in drinking water ad libitum at 0, 1, 3, and 9 ppm as Se for 14 days. At the end of Se exposure, their brains were removed and dissected into different regions. The concentration of norepinephrine (NE), dopamine (DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), serotonin (5-HT), and 5-hydroxyindolacetic acid (5-HIAA) were determined in each brain region. Food and water consumption and body weight gain were significantly decreased in the group treated with the highest concentration of sodium selenite. In mice administered sodium selenite at 3 and 9 ppm, DOPAC was significantly higher in the striatum than in the control group. The striatal HVA was also increased in the group treated with 3 ppm Se; the DA showed a similar pattern, but the increase was not statistically significant. No alterations of NE, 5-HT, or 5-HIAA levels were detected in any brain region of mice treated with sodium selenite. No significant differences in any parameter among the groups treated with selenomethionine were observed indicating that inorganic Se was more neurotoxic than organic Se via drinking water. The alterations of DA metabolites by inorganic Se in DA-rich striatum suggested a Se-specific increased neural activity of dopaminergic pathways. Results may be useful in further elucidation of neurotoxicity of Se and in establishing a safe level of intake for this element.

Selenium-induced "blind staggers" and related myths. A commentary on the extent of historical livestock losses attributed to selenosis on western US rangelands.

,~~~,~~~ Signs of acute toxicity appear in diets containing selenium in excess of 5 ~pm.’~~ A common form of acute selenosis in cattle, sheep, and pigs at present is accidental overs~pplementation.~~.~~J~~J~~J~~ Concern about spontaneous forms of selenosis reemerged in the early 1980s due to a controversy about the extent and significance of losses in waterfowl at the Kesterson Wildlife Refuge in California, following contamination of irrigation wastewater by selenium.L07J21J22 Wildlife biologists concluded that deaths and teratogenic effects in wildfowl were due to selenosis, and regulatory agencies subsequently tightened regulations intended to restrict the exposure of people, domestic animals, and wildlife to se1enium.l The Federal Drug Administration recently attempted unsuccessfully to reduce the approved level of selenium in animal feeds from 0.3 to 0.1 mg/kg (dry Amended regulations have potentially significant implications for producers in selenium-deficient areas, and for imgation district^^^,^^ and mining industrie~~~,~~,~~ in seleniferous areas. Reviewers of the extent of selenosis in people living in seleniferous areas in the United States conclude that the problem is ~are.~O.~’ A localized problem developed under unusual circumstances in people in one area of China.163 Notwith

Pathology of Experimentally Induced Chronic Selenosis (Alkali Disease) in Yearling Cattle

Prolonged oral exposure of cattle to elevated dietary selenium (Se) in forage and seleniferous plants in seleniferous areas of the western United States is associated historically with 2 clinical syndromes: alkali disease and "blind staggers." The potential for Se-induced disease in cattle and other species is considerable in areas with seleniferous shales, Se-accumulating plants, arid climates, and alkaline soils. These 2 Se-associated conditions were defined in the 1930s and 1940s, and the nosology of blind staggers is questionable. Seventeen yearling steers fed 0.15, 0.28, and 0.8 mg Se/kg body weight as selenomethionine or selenite for 120 days were euthanized and examined postmortem. Significant lesions were confined to 4 steers in the medium- and high-dose selenomethionine group and to 1 steer in the high-dose selenite group. Grossly, dystrophic hoof lesions developed in 2 steers, 1 of which had extensive separation of horn from lamellar and coronary epidermis and also lost hair from the tail switch. Histologically, tubules in the stratum medium of hooves from these 5 steers were replaced by islands of parakeratotic cellular debris, separated by more normal hoof matrix. Two of the 5 steers also had hyperplasia, acanthosis, parakeratosis, and disorganized germinal epithelium of varying severity in hoof epithelium, particularly at the tips of epidermal lamellae. These changes may distinguish the hoof lesions of chronic selenosis from those of chronic laminitis in cattle, in which dermal (chorial) changes predominate. In skin from the distal part of the tail of the animal that lost its switch, most follicles were atrophic and devoid of hairshafts and displayed dyskeratosis and mild superficial follicular keratosis. No significant lesions developed in tissues other than integument. Autometallographic staining for catalytic Se bonds in various tissues, including skin, liver, and kidney, revealed no positive staining of hair shafts; the correlation between stain intensity and dose group was poor. These findings indicate that dietary exposure for 4 months to 0.28 and 0.8 mg Se/kg in the form of selenomethionine and to 0.8 mg Se/kg in the form of sodium selenite reproduces in some cattle mild (subclinical) to severe (clinical) forms of alkali disease. No significant neurological, renal, or hepatic lesions developed, supporting the contention that blind staggers is caused by factors other than excessive dietary selenium.

Absorption of Excess Selenium and Sulfur by Plants and Animals

High concentrations of selenium (Se) and sulfur (S) often occur in overburden soils and underlying shales associated with western coal mining areas. Knowing the role of Se and S in the soil-plant-animal system is important for proper management of mine spoil reclamation. I will discuss recent findings about Se and S forms in soil, their absorption and accumulation by plants, and their subsequent toxicity to grazing animals. Selenium absorbed by the accumulating plants is metabolized to non-protein forms, while that absorbed by the non-accumulating plants occurs predominantly as selenomethionine which is readily absorbed by animals. In animals, both acute and chronic forms of selenosis are known. Death occurs when a large dose of highly-available Se is ingested. One chronic form alkali disease, produces symptoms of inappetence, hair loss, hardening and extension of nails and hooves, reduced weight gains, and poor reproductive performance. Rosenfeld and Beath identified blind staggers as another form of selenosis, but this disorder; more appropriately called polioencephalomalacia (PEM), occurs only in ruminants. However, the attribution of blind staggers (PEM) to excess Se is being questioned. Recent experimental evidence has shown that PEM is likely caused by excess sulfur. Cases of this disorder have been documented in the U.S. and Canada when ruminants have high sulfate intake from herbage and drinking water. Decisions regarding western mine reclamation should consider the potential for not only causing excess Se, but also excess sulfate in water, soil, and plants.

The Glutathione Peroxidase Reaction: Molecular Basis of the Antioxidant Function of Selenium in Mammals

This chapter presents the molecular basis of the antioxidant function of selenium in mammals. For many decades, selenium has been known as one of the most toxic elements, causing the alkali disease or blind staggers. Selenium poisoning of life stock was caused by ingestion of seleniferous plants that accumulate selenium in the form of selenium analogs of methionine, S -methylcysteine, γ-glutamylcysteine, cystathionine, or adenosylmethionine. In 1954, however, Pinsent observed that selenium promoted growth of some bacteria. Since 1957, it has been generally accepted that selenium is an essential micronutrient also for mammals. Further, incorporation of the radioactive selenium-75 into a protein fraction that co- chromatographed with glutathione (GSH) peroxidase strongly suggested that selenium is an integral part of this enzyme. Glutathione peroxidase, discovered in 1957 by Mills, had first been described as an enzyme catalyzing the reduction of H 2 O 2 by glutathione. GSH peroxidase is a homotetramer with a subunit molecular weight of about 21,000. Each subunit contains one selenium atom which, in its reduced state, is part of a selenocysteine residue. It remains to be investigated which of the many selenium deficiency syndromes observed in different animals and more recently also in humans is because of GSH peroxidase deficiency. Acute and severe selenium deficiency is obviously rare in humans and may require additional deficiencies to become critical.

Effects of single intramuscular injections of selenium at various levels to young swine.

An experiment involving 33 pigs initially weighing 18 kg, was conducted to investigate the effects of a single intramuscular injection of the effects of a single intramuscular injection of selenium (sodium selenite) at different levels on resulting blood and tissue selenium concentrations at various time intervals post-injection and to determine the effect of a single lethal injectable dosage of selenium. Serum samples were collected and analyzed for SGOT and selenium. Hepatic, kidneys and longissimus muscle tissues were collected and analyzed for selenium. The same tissues were collected from those pigs dying of selenosis. Pigs receiving selenium injections of 1.65 to 3.30 mg/kg BW died of selenosis within 4 hr to 6 days with death occurring earlier at the higher dosage levels. Symptoms in order of occurrence were: vomiting, blind staggers, foaming at the mouth, dyspnea, prostration and death. Elevated SGOT activity was observed in the remaining injected pigs at 12 hr post-injection with the enzyme activity increasing as the dosage quantity increased, suggesting mild selenium toxicosis of body tissues.

Distribution of the Meningeal Worm in White-Tailed Deer in Canada

Larvae indistinguishable from those of the meningeal worm (Pneumostrongylus tenuis) were recovered from feces of white-tailed deer (Odocoile2ls virginianus) in Quebec (63 percent), Ontario (63 percent), Manitoba (49 percent), and eastern and central Saskatchewan (9 percent) in 1971. Adult worms were found as far west as 31 miles from the Manitoba-Saskatchewan border. The parasite is established in deer of the aspen parkland, and there is no apparent barrier to its continued spread westward. MENINGEAL WORM IN DEER * Bindernagel and Anderson 1349 MUNRO, S. A. 1969. The breeding biology of the snowshoe hare during a high population in central New Brunswick. M.S. Thesis. Univ. Of New Brunswick. 85pp. NOWOSAD, R. F. 1968. An ecological study of important deer wintering areas in Nova Scotia. M.S. Thesis. Acadia Univ. 198pp. POTTER, J. G. 1965. Snow coverclimatologicaI studies No. 3. Meteorological Branch, Canada Dept. of Transport. 69pp. ROLAND, A. E. 194S. The flora of Nova Scotia. Truro Publishing Company, Truro, Nova Scotia. 552pp. RowE, J. S. 1959. Forest regions of Canada. Canada Dept. Northern Affairs and Natl. Resollrces, Forestry Branch, Bull. 123. 71pp. SHAFER, E. L., JR. 1963. The twig-count method for measuring hardwood deer browse. J. Wildl. Mgmt. 27 ( 3 ) :428437. SKINNER, W. R. 1968. Spring, summer and fall foods of the white-tailed deer in central and southern New Brunswick. M.S. Thesis. Acadia Univ. 95pp. TELFER, E. S. 1967. Comparison of moose and deer winter range in Nova Scotia. J. Wildl. Mgmt. 31(3):418-425. 1968. The status of moose in Nova Scotia. J. Mammal. 49(2):325-326. . 1971. Changes in carrying capacity of deer range in western Nova Scotia Cranadian Field-Naturalist 85(3):231-234. Received for publication December 27, 1971. New Brunswick (Smith and Archibald 1967). All of these records are from deer in the deciduous forest or coniferous forest biome or in the ecotone between these two biomes. In 1964, the meningeal worm was shown to be the causal agent of neurologic disease in moose ( Alces alces ), more commonly known as moose sickness or blind staggers (Anderson 1964). Since then, specimens of the meningeal worm have been recovered from the brain or spinal cord of moose with neurologic disease from the Fort Frances district of northwestern Ontario (Anderson 1965 ), Nova Scotia and New Brunswick (Smith et al. 1964, Smith and Archibald 1967), Maine (Behrend and Witter 1968), The nematode Pneumostrongylus tenuis, first described from white-tailed deer in New York State ( Dougherty 1945 ), has been reported in the United States from deer in Michigan ( Degiusti [DeGiusti] l9SS, 1963 ), Pennsylvania ( Alibasoglu et al. 1961, Samuel and Beaudoin 1966), western Virginia (Dudak et al. 1966), Minnesota ( Karns l967 ), Maine ( Behrend and Witter 1968), and Wisconsin (Samuel and Trainer 1969). It has also been reported from 12 states of the southeastern United States as far west as Arkansas and as far north as Maryland ( Prestwood and Smith 1969 ) . In Canada, it is known from the provinces of Ontario (Anderson 1963), Nova Scotia, and This content downloaded from 207.46.13.43 on Wed, 25 May 2016 05:34:58 UTC All use subject to http://about.jstor.org/terms 1350 Journal of Wildlife Management, Vol. 36, No. 4, October 1972 the parasite occurring west of southeastern Manitoba was a matter of speculation. The present study was undertaken to determine the distribution of the meningeal worm in Ganada west of New Brunswick. Our study was based primarily on the recovery of firststage larvae from deer pellet groups but was supported by the examination of heads from critical areas. This study was supported by funds from the Canadian National Sportsman's Show. We thank the personnel of the Quebec Wildlife Service, the Ministry of Natural Resources, the Manitoba Department of Mines, Resources and Environmental Management, and the Saskatchewan Department of Natural Resources for their assist-

Toxicity of Swainsona canescens for sheep in Western Australia

The botanical description and distribution of a Western Australian species of Swainsona is reported in connection with investigations of the plant as a poison plant responsible for extensive losses of sheep and horses in the Goldfields station country. Feeding trials in sheep and rabbits confirmed the toxicity of Swainsona. Sheep exhibited depression, anxiety, "blind staggers", incordination, and emaciation. The central nervous system of both animal species was seriously affected, with chromatolytic and vacuolar degeneration of neurones and with oedematous changes. Renal cells showed hydropic degeneration and spleens were intensely haemosiderotic. These changes occurred after 4 or 5 weeks of chronic feeding and closely resembled those of locoweed poisoning of livestock in the western United States.

Growth Responses to Selenium in Lambs

Abstract Extract Until recently, selenium as a dietary constituent was regarded as of importance only where it occurs in excess of certain well defined limits. When these limits are exceeded, selenium toxicity develops, either in the acute form; in the subacute form, called “blind staggers”, following the ingestion of seleniferous weeds; or in the chronic form, called “alkali disease”, caused by the prolonged grazing of pasture or forage crops containing smaller amounts of selenium. In selenium poisoning areas, about 5 p.p.m. in herbage is considered to be the tolerance limit for ,livestock. Smaller amounts have been estimated to be dangerous in man (Garner, 1957).

Growth responses to selenium in lambs

Abstract Extract Until recently, selenium as a dietary constituent was regarded as of importance only where it occurs in excess of certain well defined limits. When these limits are exceeded, selenium toxicity develops, either in the acute form; in the subacute form, called “blind staggers”, following the ingestion of seleniferous weeds; or in the chronic form, called “alkali disease”, caused by the prolonged grazing of pasture or forage crops containing smaller amounts of selenium. In selenium poisoning areas, about 5 p.p.m. in herbage is considered to be the tolerance limit for ,livestock. Smaller amounts have been estimated to be dangerous in man (Garner, 1957).

Selenomethionine in enzymatic transmethylations.

IN the past, biological interest in selenium has been centred around its toxic role as the cause of ‘alkali disease’ and ‘blind staggers’1 and as a source of industrial poisoning2. However, recent developments suggest a more important role for this element. Thus, it has been shown that selenium is an essential trace element for the rat3 and is stimulatory, if not essential, for the growth of certain plants4. While inorganic selenium compounds are active in these cases, there is evidence that these inorganic selenium compounds are converted biologically into organic compounds, including the selenium analogues of cysteine5, cystine, methionine6 and cystathionine7. The structure of the essential selenium compound or compounds, therefore, remains to be established.

Selenium as a Health Hazard

IT is USEFUL to recall that selenium is a congener of sulphur, tellurium and arsenic. Selenium is a rare element, being slightly more abundant than gold, but is found neither in large quantities nor in the elemental form. The principal sources are flue-dusts from sulphuric acid works using seleniferous pyrites, flue-dusts from smelting processes and particularly the anode sludge of the electrolytic refinement of copper which may contain up to 15 per cent. Its current price is £12 per lb. Traces of selenium occur in rocks or soils all over the world. The mesozoic soils of the great plains of the U.S.A. (Dakota, Montana, Wyoming) have concentrations up to 30 parts per million, and plants growing in such soils absorb selenium which may subsequently be ingested by animals and humans in amounts sufficient to give rise to chronic and sometimes to fatal poisoning. Wheat grown on soil containing 30 parts per million may be toxic even after milling, though the toxicity is mainly associated with the protein moiety. Cattle and horses grazing on soils with concentrations of 10-20 parts per million may be the subjects of chronic poisoning. This, in horses, is shown by a loss of mane and tail hair and by abnormal hoof growth. In more severe cases, horses may develop blind staggers, erosion of bone, focal neurosis of liver, with cirrhosis—if of long standing—and death from respiratory failure.' The danger of seleniferous soils is minimised by high rainfall and possibly by the presence of arsenic, which in traces may inhibit the toxic effects of selenium. There is little evidence that selenium of vegetable origin is ingested in injurious quantities by man, but it can be found concentrated in the lungs, liver, kidney and spleen. Normal urine contains minute amounts, the principal source of which is peas and beans. Selenium intake predisposes to dental caries; the garlicky odour of the breath is due to dimethyl selenide. The industrial uses of selenium have increased rapidly in recent years. The common commercial forms are grey metallic selenium and selenium dioxide. These are used in 1, rectifiers, to convert an alternating current to direct as required for battery charging or electrolytic processes,

Administration of BAL in selenium poisoning.

Selenium causes “alkali disease” or “blind staggers” in livestock in the Dakotas, Kansas, Montana, Wyoming, and other Western States where the soil and vegetation are high in selenium content. Therefore the toxic properties of selenium and its compounds are of great importance in these areas. As far as we know, there is no reliable agent which is of value in preventing or curing the symptoms of selenium poisoning, though protective action of arsenic has been demonstrated by Moxon et al. Peters, Stocken, and Thompson described the effectiveness of BAL in counteracting the effects of arsenical poisoning. The protective action of this compound in arsenical poisoning was believed to be due to the release of SH groups by BAL which could compete with the tissue SH groups for the arsenic, and act as a detoxifying agent. The nature of the reaction between arsenic and BAL made it seem probable that BAL would react similarly with other metals, and Gilman, Allen, and Philips have reported its effectiveness as an antidote for bichloride of mercury and cadmium poisoning, and Braun, Lusky, and Calvery showed similar results against poisoning by antimony, bismuth, chromium and nickel. However, they demonstrated that lead and selenium were made more toxic by BAL. Our experiments performed using BAL as an antagonist against selenium poisoning confirmed the results already described However, we have found no explanation in the literature of the apparent synergism between BAL and selenium, hence our work has been directed along this line. Experimental. Healthy white rats 6 to 8 weeks old, 120 and 150 g of weight were used. Selenium was administered by intraperitoneal injections in the form of a freshly prepared aqueous solution of sodium selenite (SS).

SELENIUM POISONING

ArticlesSELENIUM POISONINGAlvin L. Moxon, and Morris RhianAlvin L. Moxon, and Morris RhianPublished Online:01 Oct 1943https://doi.org/10.1152/physrev.1943.23.4.305MoreSectionsPDF (5 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByAcute oral selenium intoxication with ten times the lethal dose resulting in deep gastric ulcerThe Journal of Emergency Medicine, Vol. 26, No. 2The nutritional significance, metabolism and toxicology of selenomethionineThe Epidemiology of Selenium and Human Cancer16 April 2018 | Tumori Journal, Vol. 86, No. 2Selenium-induced “Blind Staggers” and Related Myths. A Commentary on the Extent of Historical Livestock Losses Attributed to Selenosis on Western US Rangelands26 June 2016 | Veterinary Pathology, Vol. 33, No. 1Investigation of Selenium Sources Associated with Chronic Selenosis in Horses of Western Iowa25 June 2016 | Journal of Veterinary Diagnostic Investigation, Vol. 5, No. 1Estimation of waterborne selenium concentrations that are toxicity thresholds for wildlifeArchives of Environmental Contamination and Toxicology, Vol. 23, No. 2Acute toxicity and urinary excretion of diphenyldiselenideToxicology Letters, Vol. 48, No. 3Selenium compounds in the fathead minnow (Pimephales promelas)—I. Uptake, distribution, and elimination of orally administered selenate, selenite and l-selenomethionineComparative Biochemistry and Physiology Part C: Comparative Pharmacology, Vol. 83, No. 1Selenium compounds in the fathead minnow (Pimephales promelas)—II. Quantitative approach to gastrointestinal absorption, routes of elimination and influence of dietary pretreatmentComparative Biochemistry and Physiology Part C: Comparative Pharmacology, Vol. 83, No. 1Selenium Toxicity in Animals with Emphasis on Man5 September 2016 | Journal of the American College of Toxicology, Vol. 5, No. 1A correlation between selenium accumulation in sunfish and changes in condition factor and organ weightEnvironmental Pollution Series A, Ecological and Biological, Vol. 34, No. 4Reduction of deer browsing of Douglas-fir (Pseudotsuga menziesii) seedlings by quadrivalent seleniumForest Ecology and Management, Vol. 7, No. 3In vitro hemolysis of rat erythrocytes by selenium compoundsBiochemical Pharmacology, Vol. 32, No. 6Haemolysis of normal and glutathione-deficient sheep erythrocytes by selenite and telluriteBiochemical Pharmacology, Vol. 30, No. 18Selenium in the environmentScience of The Total Environment, Vol. 17, No. 1Interactions between mercuric chloride and sodium selenite on cultured rat cerebrumToxicology Letters, Vol. 6, No. 3Toxicological effect of selenium on fishEnvironmental Pollution Series A, Ecological and Biological, Vol. 21, No. 3Metabolic interrelationships between arsenic and seleniumEnvironmental Health Perspectives, Vol. 19Pharmacology and toxicology of heavy metals: SeleniumPharmacology & Therapeutics. Part A: Chemotherapy, Toxicology and Metabolic Inhibitors, Vol. 1, No. 2The sensitivity of function tests in detecting liver damage in the ratToxicology and Applied Pharmacology, Vol. 28, No. 3THE SOCIAL FATE OF THE AMPUTEEThe Lancet, Vol. 298, No. 7737IS SELENIUM A TERATOGEN ?The Lancet, Vol. 298, No. 7737TREATMENT OF CARBON-MONOXIDE POISONINGThe Lancet, Vol. 295, No. 7645PRESSURE ON G.M.C.The Lancet, Vol. 295, No. 7645SELENIUM—A POSSIBLE TERATOGEN?The Lancet, Vol. 295, No. 7645The effect of selenous acid on the hematopoietic system of chicken embryosToxicology and Applied Pharmacology, Vol. 11, No. 3Selenium metabolismToxicology and Applied Pharmacology, Vol. 9, No. 1Selenium metabolismToxicology and Applied Pharmacology, Vol. 9, No. 1Abnormal trace metals in man—VanadiumJournal of Chronic Diseases, Vol. 16, No. 10Effects of sodium selenite on several blood componentsToxicology and Applied Pharmacology, Vol. 5, No. 2Some effects of sodium selenite on the cardiovascular systemToxicology and Applied Pharmacology, Vol. 2, No. 1INFLUENCE OF SULFUR ON THE TOXICITY OF SELENIUM TO ASPERGILLUS1 June 1955 | American Journal of Botany, Vol. 42, No. 6TOXIPATHIC AND TROPHOPATHIC HEPATITISThe Lancet, Vol. 243, No. 6293 More from this issue > Volume 23Issue 4October 1943Pages 305-337 https://doi.org/10.1152/physrev.1943.23.4.305History Published online 1 October 1943 Published in print 1 October 1943 Metrics