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1984
DOI: 10.2527/jas1984.5851216x
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Effect of Inorganic Selenium Supplementation on Selenosis in Postweaning Swine

Abstract: A total of 72 pigs weaned at 4 wk of age were allotted by litter and weight to nine treatment groups and fed 20% protein cornsoybean meal diets supplemented with various levels of inorganic Se during a 37-d postweaning period. Eight groups were fed diets with 0, 2.5, 5.0, 7.5, 10, 15, 20 or 40 ppm Se provided as sodium selenite, while a ninth was offered the 0- and 40-ppm Se diets in separate feeders. Gains and feed intakes were similar during the trial for the 0- and 2.5-ppm Se diets. Both gain and feed intak… Show more

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Cited by 42 publications
(40 citation statements)
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“…A doença ocorre, principalmente, em suínos jovens, entre um e cinco meses de idade. São descritas três apresentações clínicas distintas desta enfermidade: dificuldades locomotoras com paresia dos membros e tetraparesia, resultantes de poliomielomalácia simétrica focal (Wilson et al 1983, Carson 2006; lesões de pele e separação da borda coronária dos cascos (Mahan & Moxon 1984, Banholzer & Heinrtzi 1998, Hélie et al 1998); e perdas reprodutivas caracterizadas por diminuição da concepção e natimortos (Carson 2006). Em alguns surtos foram descritas as lesões nos cascos concomitante as lesões medulares (Harrison et al 1983, Castell et al 1985, Casteignau et al 2006.…”
Section: Introductionunclassified
“…A doença ocorre, principalmente, em suínos jovens, entre um e cinco meses de idade. São descritas três apresentações clínicas distintas desta enfermidade: dificuldades locomotoras com paresia dos membros e tetraparesia, resultantes de poliomielomalácia simétrica focal (Wilson et al 1983, Carson 2006; lesões de pele e separação da borda coronária dos cascos (Mahan & Moxon 1984, Banholzer & Heinrtzi 1998, Hélie et al 1998); e perdas reprodutivas caracterizadas por diminuição da concepção e natimortos (Carson 2006). Em alguns surtos foram descritas as lesões nos cascos concomitante as lesões medulares (Harrison et al 1983, Castell et al 1985, Casteignau et al 2006.…”
Section: Introductionunclassified
“…However, the clinical presentation, necropsy findings, elimination pattern of blood selenium, and tissue selenium residues found at slaughter were consistent with those aspects of most experimental studies and field investigations of accidental selenium toxicosis. 1,2,4,[9][10][11][12][13][14][15][17][18][19]21,[23][24][25][26]28,30,[32][33][34][35][36][37] Clinical signs of selenium toxicosis (alopecia, reduced weight gain, hoof lesions) were apparent in 75% of affected pigs and were similar to signs observed in previously described experimental and accidental intoxications. 1,4,[9][10][11][12]15,[23][24][25]28,30,[34][35][36] Death of 30% (88/300) of feeder pigs accidentally exposed to feed containing a mean of 19 ppm (dry weight) sodium selenite for 42 days was previously reported.…”
Section: Discussionmentioning
confidence: 59%
“…In cases of chronic selenium toxicosis in swine where high concentrations of sodium selenite have been the cause, liver has been shown to be the organ with the highest concentration of selenium. 9,21,23,24 Although 1 liver had elevated selenium 72 days after withdrawal of contaminated feed, it is unlikely that there would have been a food safety risk to human beings. Daily dietary recommendations for selenium vary from 40 g/person/day, 20,22 which is a recommended daily allowance of 0.87 g/kg/day 6 (70 g for a 79-kg person), to a maximum acceptable intake of 500 g/person/day.…”
Section: Discussionmentioning
confidence: 99%
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