Comparative Toxicity of Selenium from Seleno-DL-methionine, Sodium Selenate, and <i>Astragalus bisulcatus</i> in Pigs

Panter, Kip E.; Hartley, W. J.; James, Lynn F.; Mayland, H. F.; Stegelmeier, B. L.; Kechele, P. O.

doi:10.1093/toxsci/32.2.217

Cited by 43 publications

(43 citation statements)

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“…Os achados clínicos e patológicos dos surtos aqui descritos são compatíveis com os casos de intoxicação espontânea e experimental por selênio em suínos (Harrison et al 1983, Wilson et al 1983, 1988, 1989, Castell et al 1985, Saford 1990, Stowe et al 1992, Schultz & Hoffmann 1995, Panter et al 1996, Penrith & Robinson 1996, Banholzer & Heinritzi 1998, Davidson-York et al 1999, Casteignau et al 2006, Nathues et al 2010. Os achados histológicos sugerem um diagnóstico provável de intoxicação por selênio, pois o excesso de ingestão de selênio é a única causa conhecida de poliomielomalácia simétrica focal em suínos (Wilson et al 1983(Wilson et al , 1988.…”

Section: Discussionunclassified

“…Após 42 dias da retirada da ração os suínos que não morreram apresentaram níveis hepáticos de selênio inferiores a 1,73ppm, o que difere dos achados de Davidson-York et al (1999) que, após 72 dias da retirada da ração com excesso de selênio, ainda detectaram um animal com nível de 3,3ppm de Se no fígado. Não foi observada correlação entre altos níveis de selênio no fígado e a severidade das lesões histológicas, dados semelhantes aos encontrados na literatura (Panter et al 1996, Davidson--York et al 1999. A porcentagem de animais com paralisia nos surtos variou de 15 a 16%, dados semelhantes já foram descritos (Davidson-York et al 1999).…”

Section: Discussionunclassified

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Intoxicação por selênio em suínos no Sul do Brasil

et al. 2014

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RESUMO.-São descritos dois surtos de intoxicação por selênio em suínos na região Sul do Brasil. Foram acometidos leitões em fase de creche, entre 27 e 22 dias, com mortalidade variando de 16% a 15,3% (Surto 1 e 2 respectivamente). Os suínos apresentaram poliomielomalacia simétrica focal e lesões de casco, que inicialmente eram caracterizadas por uma linha avermelhada na borda coronária que evoluía nos suínos sobreviventes para desprendimento do casco. Os sinais clínicos iniciaram após seis dias (Surto 1) e 30 horas (Surto 2) da introdução da ração com alto teor de selênio. O surgimento dos sinais foi abrupto, caracterizado por andar cambaleante, com evolução para paralisia dos membros pélvicos e posteriormente tetraparesia. Macroscopicamente observaram-se focos circulares amarelados com áre-as deprimidas mais escuras, restritas ao corno ventral da substância cinzenta em intumescências cervical e lombar. Microscopicamente essas áreas corresponderam à malacia da substância cinzenta, caracterizada por microcavitações, perda neuronal, cromatólise, neuronofagia, infiltrado de células Gitter, microgliose, astrócitos de Alzheimer tipo II e proliferação de células endoteliais evidenciadas na imunohistoquímica (IHQ) para fator de von Willebrand. Ainda, Two outbreaks of poisoning by selenium in swine in southern Brazil are described. Piglets were affected in the post-weaning period, between 27 and 22 days, with mortality rates ranging from 16% to 15.3% (Outbreak 1 and 2 respectively). The pigs had focal symmetrical poliomielomalacia and hoof lesions, which were initially characterized by a reddish line at the coronary band that evolved in surviving pigs to release of the hooves. Clinical signs were observed after six days (Outbreak 1) and 30h (Outbreak 2) after the introduction of feed with high selenium content. The appearance of the signs was abrupt, characterized by gait and progressing to paralysis of the hind limbs and later to tetraparesis. Macroscopically, in some animals there were yellow circular foci with darker areas restricted to the ventral horn of the gray matter in the cervical and lumbar intumescence. Microscopically, these areas correspond to gray matter malacia, characterized by microcavitation, neuronal loss, chromatolysis, neuronophagia, infiltrating Gitter cells, microgliosis, Alzheimer's type II astrocytes and proliferation of endothelial cells which were labeled by immunohistochemistry (IHC) as von Willebrand factor. Also in the second outbreak, two pigs showed diffuse vacuolation of the cytoplasm of neurons and in one pig gemistocytic astrocytes were observed. In IHC for GFAP astrocytosis and astrogliosis was observed. Besides those spinal changes in two pigs symmetrical polioencephalomalacia in the brainstem was found. In feed samples, 3.38ppm (Outbreak 1) and 154ppm (Outbreak 2) of Se/kg were detected, and in liver samples higher dosages than 3.34ppm (range from 3.34 to 10ppm) were found. In Outbreak 2, 44 days after the withdrawal of the diet, the euthanasia of six pigs was performed to monitor ...

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Section: Discussionunclassified

Intoxicação por selênio em suínos no Sul do Brasil

et al. 2014

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“…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: 56%

“…A recent study has confirmed this finding. 28 Among-pig variation in feed intake, length of time on contaminated feed, and length of time between feed removal and initial blood test may have been factors that contributed to these findings. A relationship between selenium concentration in the feed and blood selenium concentration in the control pigs did exist, similar to that in previous reports.…”

Section: Discussionmentioning

confidence: 95%

“…32 Experimental trials describing both the clinical effects and the tissue concentrations of selenium in ex- Received for publication May 19, 1997. perimentally intoxicated swine are well documented. 1,2,[9][10][11][12]14,17,21,23,28,37 Accidental selenium toxicosis in swine has also been widely reported, 13,15,25,30,[34][35][36] but little information is available concerning elimination of selenium from blood and tissues in field outbreaks involving multiple premises and various feed selenium concentrations in affected pigs. The purpose of this study was to describe clinical, pathologic, and epidemiologic features of an outbreak of selenium toxicosis in 24 swine herds and to monitor selenium elimination from blood and tissues of affected pigs to estimate an appropriate slaughter withdrawal time.…”

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confidence: 99%

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Selenium Elimination in Pigs after an Outbreak of Selenium Toxicosis

et al. 1999

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Abstract. In May 1996, 150 grower pigs in 5 California counties were exposed to selenium-contaminated feed distributed by a single feed company. Feed samples from 20 herds had a mean selenium concentration of 121.7 ppm dry weight (range, 22.1-531 ppm). In San Luis Obispo County, 52 pigs in 24 herds were exposed to the feed, and 8 pigs died with signs of paralysis. Bilateral symmetrical poliomyelomalacia involving the ventral horns of the cervical and lumbar intumescence was evident on histologic examination of spinal cord from affected pigs. Of 44 surviving exposed pigs, 33 (75%) exhibited signs of selenosis, including anorexia, alopecia, and hoof lesions. Thirty-nine of 44 pigs (88.6%) had elevated (Ͼ1 ppm) blood selenium concentrations. Surviving exposed pigs were changed to a standard commercial ration containing approximately 0.5 ppm (dry weight) selenium. Blood selenium concentrations were determined weekly for 46 days following removal of the contaminated feed and were compared with values of 20 control pigs fed a standard commercial ration. Mean (ϮSD) blood selenium concentrations of exposed pigs were 3.2 Ϯ 2.6 ppm at the initial sampling and 0.4 Ϯ 0.1 ppm after 46 days. Mean blood selenium concentrations of Յ 0.3 ppm for control pigs at all samplings were significantly lower (P Ͻ 0.001) than concentrations for exposed pigs. Muscle and liver samples of 22 of the 44 exposed pigs were collected at slaughter approximately 72 days after withdrawal of the selenium-contaminated feed. Muscle samples had a mean selenium concentration of 0.36 ppm (wet weight). Liver samples had a mean selenium concentration of 1.26 ppm (wet weight). One liver sample had a selenium value in the toxic range for pigs (3.3 ppm wet weight; reference range, 0.4-1.2 ppm). A 1-compartment pharmacokinetic model of selenium elimination in exposed pigs was generated, and the geometric mean blood selenium elimination half-life was estimated to be 12 days. The 60-day withdrawal time recommended by the Food Animal Residue Avoidance Database was considered sufficient to allow safe human consumption of tissues from exposed pigs.Selenium is an essential trace element for swine, necessary for cells to detoxify peroxides. 29 It is one of the most toxic trace elements 26,33 and has a narrow margin of safety. Toxicosis has been reported in swine after repeated ingestion of feed containing Ͼ5 ppm selenium (dry weight). 4,12,[24][25][26] Signs of selenium toxicosis in swine include anorexia, alopecia, separation of hoof and skin at the coronary band, degenerative changes in the liver and kidney, and poliomyelomalacia. 16,26,27,33 In 1974, the US Food and Drug Administration (FDA) authorized the addition of a sodium salt of selenium to swine feed at a concentration of 0.1 ppm (dry weight) in the complete ration. 32 Current FDA regulations allow a maximum of 0.3 ppm (dry weight) in the complete ration as either inorganic sodium selenite or selenate. 7 Sodium selenite is the most commonly used selenium compound in domestic feed because of its lower cost, a...

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