Diagnostic Criteria for Selenium Toxicosis in Aquatic Birds: Dietary Exposure, Tissue Concentrations, and Macroscopic Effects

Albers, Peter H.; Green, D. Earl; Sanderson, Caroline J.

doi:10.7589/0090-3558-32.3.468

Cited by 44 publications

(30 citation statements)

References 33 publications

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“…Some, but not all, of the lesions described in the high dose great egrets were similar to those in ducks fed seleno-DLmethionine (Albers et al, 1996;Green and Albers, 1997). Liver selenium concentrations in the ducks were similar to birds in our study (Spalding et al, 2000).…”

Section: Histology Of Other Organssupporting

confidence: 75%

Histologic, Neurologic, and Immunologic Effects of Methylmercury in Captive Great Egrets

Spalding

Frederick

McGill

et al. 2000

Journal of Wildlife Diseases

115

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Captive great egret (Ardea albus) nestlings were maintained as controls or were dosed with methylmercury chloride at low (0.5), and high doses (5 mg/kg, wet weight) in fish. Low dosed birds were given methylmercury at concentrations comparable to current exposure of wild birds in the Everglades (Florida, USA). When compared with controls, low dosed birds had lower packed cell volumes, dingy feathers, increased lymphocytic cuffing in a skin test, increased bone marrow cellularity, decreased bursal wall thickness, decreased thymic lobule size, fewer lymphoid aggregates in lung, increased perivascular edema in lung, and decreased phagocytized carbon in lung. High dosed birds became severely ataxic and had severe hematologic, neurologic, and histologic changes. The most severe lesions were in immune and nervous system tissues. By comparing responses in captive and wild birds, we found that sublethal effects of mercury were detected at lower levels in captive than in wild birds, probably due to the reduced sources of variation characteristic of the highly controlled laboratory study. Conversely, thresholds for more severe changes (death, disease) occurred at lower concentrations in wild birds than in captive birds, probably because wild birds were exposed to multiple stressors. Thus caution should be used in applying lowest observed effect levels between captive and wild studies.

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Section: Histology Of Other Organssupporting

confidence: 75%

Histologic, Neurologic, and Immunologic Effects of Methylmercury in Captive Great Egrets

Spalding

Frederick

McGill

et al. 2000

Journal of Wildlife Diseases

115

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“…2b), shown similar accumulation pattern in tissues. Selenium was preferentially accumulated in the kidney of the turtles from both SeMet groups and was consistent with other studies in reptiles (Hopkins et al 2002 but differed from those in birds which reported a preferential hepatic storage of selenium (Albers et al 1996;Franson et al 2007). Differences in selenium kinetics between birds and turtles were further indicated in blood and muscle.…”

Section: Selenium Kineticssupporting

confidence: 90%

Toxicokinetics of selenium in the slider turtle, Trachemys scripta

et al. 2016

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Selenium (Se) is an essential element that can be harmful for wildlife. However, its toxicity in poikilothermic amniotes, including turtles, remains poorly investigated. The present study aims at identifying selenium toxicokinetics and toxicity in juvenile slider turtles (age: 7 months), Trachemys scripta, dietary exposed to selenium, as selenomethionine SeMet, for eight weeks. Nondestructive tissues (i.e. carapace, scutes, skin and blood) were further tested for their suitability to predict selenium levels in target tissues (i.e. kidney, liver and muscle) for conservation perspective. 130 juvenile yellow-bellied slider turtles were assigned in three groups of 42 individuals each (i.e. control, SeMet 1 and SeMet 2 ). These groups were subjected to a feeding trial including an eight-week supplementation period SP 8 and a following 4-week elimination period EP 4 . During the SP 8 , turtles fed on diet containing 1.1 ± 0.04, 22.1 ± 1.0 and 45.0 ± 2.0 lg g -1 of selenium (control, SeMet 1 and SeMet 2 , respectively). During the EP 4 , turtles fed on non-supplemented diet. At different time during the trial, six individuals per group were sacrificed and tissues collected (i.e. carapace, scutes, skin, blood, liver, kidney, muscle) for analyses. During the SP 8 (Fig. 1), both SeMet 1 and SeMet 2 turtles efficiently accumulated selenium from a SeMet dietary source. The more selenium was concentrated in the food, the more it was in the turtle body but the less it was removed from their tissues. Moreover, SeMet was found to be the more abundant selenium species in turtles' tissues. Body condition (i.e. growth in mass and size, feeding behaviour and activity) and survival of the SeMet 1 and SeMet 2 turtles seemed to be unaffected by the selenium exposure. There were clear evidences that reptilian species are differently affected by and sensitive to selenium exposure but the lack of any adverse effects was quite unexpected.

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“…Mortality (10%) and histopathological effects, including bile duct hyperplasia and hemosiderin pigmentation of the liver and spleen, occurred in the 32 ppm group. Other studies developed diagnostic criteria for selenium toxicosis with DL-selenomethionine (0, 10, 20, 40, or 80 ppm Se) in the diet of adult mallards for 16 weeks (Albers et al, 1996;Green and Albers, 1997). Mortality was 5, 14, and 100% in the 20, 40, and 80 ppm groups, respectively.…”

Section: Adult Mallardsmentioning

confidence: 99%

Selenium toxicity: cause and effects in aquatic birds

Spallholz

Hoffman²

2002

Aquatic Toxicology

214

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There are several manners in which selenium may express its toxicity: (1) an important mechanism appears to involve the formation of CH 3 Se − which either enters a redox cycle and generates superoxide and oxidative stress, or forms free radicals that bind to and inhibit important enzymes and proteins. (2) Excess selenium as selenocysteine results in inhibition of selenium methylation metabolism. As a consequence, concentrations of hydrogen selenide, an intermediate metabolite, accumulate in animals and are hepatotoxic, possibly causing other selenium-related adverse effects. (3) It is also possible that the presence of excess selenium analogs of sulfur-containing enzymes and structural proteins play a role in avian teratogenesis. L-selenomethionine is the most likely major dietary form of selenium encountered by aquatic birds, with lesser amounts of L-selenocysteine ingested from aquatic animal foods. The literature is suggestive that L-selenomethionine is not any more toxic to adult birds than other animals. L-Selenomethionine accumulates in tissue protein of adult birds and in the protein of egg white as would be expected to occur in animals. There is no suggestion from the literature that the levels of L-selenomethionine that would be expected to accumulate in eggs in the absence of environmental concentration of selenium pose harm to the developing embryo. For several species of aquatic birds, levels of Se as selenomethionine in the egg above 3 ppm on a wet weight basis result in reduced hatchability and deformed embryos. The toxicity of L-selenomethionine injected directly into eggs is greater than that found from the entry of L-selenomethionine into the egg from the normal adult diet. This suggests that there is unusual if not abnormal metabolism of L-selenomethionine in the embryo not seen when L-selenomethionine is present in egg white protein where it likely serves as a source of selenium for glutathione peroxidase synthesis in the developing aquatic chick.

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Diagnostic Criteria for Selenium Toxicosis in Aquatic Birds: Dietary Exposure, Tissue Concentrations, and Macroscopic Effects

Cited by 44 publications

References 33 publications

Histologic, Neurologic, and Immunologic Effects of Methylmercury in Captive Great Egrets

Histologic, Neurologic, and Immunologic Effects of Methylmercury in Captive Great Egrets

Toxicokinetics of selenium in the slider turtle, Trachemys scripta

Selenium toxicity: cause and effects in aquatic birds

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