Tolerance Levels of Seleniferous Grains in Laying Rations

Poley, W. E.; Moxon, A. L.

doi:10.3382/ps.0170072

Cited by 39 publications

(12 citation statements)

References 3 publications

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“…Other deformities found at Kesterson NWR included hydrocephaly, microphthalmia and anophthalmia, amelia and hemimelia, as well as foot and toe defects characterized by ectrodactyly and abbreviated or twisted metatarsi. Multiple malformations of the extremities have been reported in chickens following dietary exposure of 5-15 ppm Se from naturally occurring seleniferous grains containing Se probably as selenomethionine (Poley et al, 1937;Poley and Moxon, 1938). Studies that examined the effects of sodium selenite in the diet of chickens revealed embryotoxicity and poor hatching success without a high level of teratogenicity (Thapar et al, 1969;Arnold et al, 1972;Ort and Latshaw, 1978).…”

Section: Discussionmentioning

confidence: 97%

“…Early studies using naturally contaminated grains from seleniferous locations revealed that grain containing 2.5 ppm Se fed to chickens had no effect on egg hatchability, 5.0 ppm had some effect, but 10 ppm reduced hatchability to zero (Poley and Moxon, 1938). Studies with sodium selenite in the diet also demonstrated reduced hatchability in chickens receiving 5-8 ppm Se (Thapar et al, 1969;Arnold et al, 1972;Ort and Latshaw, 1978) and in Japanese quail {Coturnix japonica) with 6-12 ppm (El-Begearmi et al, 1977).…”

Section: Introductionmentioning

confidence: 92%

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Embryotoxic and teratogenic effects of selenium in the diet of mallards

Hoffman¹,

Heinz²

1988

Journal of Toxicology and Environmental Health

116

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Mallards (Anas platyrhynchos) were fed a control diet, diets containing 1, 5, 10, or 25 ppm Se as sodium selenite, or a diet containing 10 ppm Se as seleno-DL-methionine in the first of two experiments. Selenium at 10 ppm as selenomethionine or 25 ppm as sodium selenite caused a 40-44% decrease in the total number of eggs that hatched compared to controls. Selenium at 25 ppm (sodium selenite) resulted in a 19% decrease in mean embryonic weight at 18 d of incubation, accompanied by a 6% decrease in crown-rump length. Ten parts per million Se as selenomethionine was more teratogenic than sodium selenite at 25 ppm. Selenomethionine (10 ppm Se) resulted in an incidence of 13.1% malformations that were often multiple, whereas sodium selenite (10 and 25 ppm Se) resulted in 3.6 and 4.2% malformations. The teratogenicity of selenomethionine was confirmed in a second experiment in which mallards received 1, 2, 4, 8, or 16 ppm Se as selenomethionine, resulting in 0.9, 0.5, 1.4, 6.8, and 67.9% malformations, respectively. These malformations included hydrocephaly, microphthalmia, lower bill defects, and foot defects with ectrodactyly. Both forms of selenium increased the incidence of edema and stunted embryonic growth. Selenomethionine (10 ppm Se) resulted in a significant increase of approximately 40% in plasma glutathione peroxidase activity and a 70% increase in sorbitol dehydrogenase activity (indicative of hepatotoxicity) in hatchlings. Sodium selenite (25 ppm Se) resulted in fourfold elevation in plasma uric acid concentration, indicative of renal alteration. Selenomethionine accumulated much better in eggs than did sodium selenite. These findings indicate that selenomethionine is considerably more teratogenic and generally more embryotoxic than sodium selenite, probably due to higher uptake of selenomethionine.

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 92%

Embryotoxic and teratogenic effects of selenium in the diet of mallards

Hoffman¹,

Heinz²

1988

Journal of Toxicology and Environmental Health

116

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“…Studies conducted with poultry in the 1930s and ducks in the 1980s and 1990s conclusively demonstrated that birds are sensitive to the toxic effects of selenium-contaminated feed (Poley and Moxon, 1938;Poley et al, 1941;Heinz et al, 1987;Gold, 1988, 1989;Hoffman and Heinz, 1988;Heinz and Fitzgerald, 1993;Stanley et al, 1994). These studies suggest a reproductive effects threshold of about 5 mg/kg-dry weight (mg/kg dw) in the diet for sensitive bird species, such as mallards (Anas platyrhynchos) (Table 1).…”

Section: Introductionmentioning

confidence: 92%

Egg Selenium Concentrations as Predictors of Avian Toxicity

Fairbrother

Brix

Toll

et al. 1999

Human and Ecological Risk Assessment: An International Journal

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a ecological planning and toxicology, inc., 5010 SW Hout St., Corvallis, OR 97333-9540 ABSTRACT Aquatic birds are exposed to selenium through their diet by ingesting aquatic invertebrates that have accumulated selenium from water and the food chain. However, dietary composition is highly variable among species, over time, and across sites, making it difficult to provide accurate estimations of dietary exposure for particular species at specific locations. Selenium accumulates in the egg, resulting in embryo malformation, embryonic death, and decreased survival of juveniles. If the relationship between egg concentration and these reproductive parameters can be defined with sufficient certainty, then risk assessments can be performed through analysis of egg selenium concentrations. Other researchers have proposed egg toxicity thresholds that lead to conclusions of widespread selenium toxicoses in waterbirds. However, we believe these values are overly conservative and that it is unlikely that selenium is posing a significant risk to wild birds in areas where the current water quality criterion is being met. Through the use of simple statistical models (logit, probit, and Weibull functions) we are able to express mortality and teratogenicity relationships for mallards (Anas platyrhynchos) in such a manner that the risk manager can be presented with information about the probability of reduced duckling survival if mean egg selenium (MES) concentrations are known. Data analysis indicates that the two endpoints (mortality * Corresponding author: Dr. Anne Fairbrother, ecological planning and toxicology, inc., 5010 SW Hout St., Corvallis, OR 97333-9540;Fairbrother, et al.and teratogenesis) cannot be distinguished statistically. Commonly used effects thresholds (the EC 10 and EC 20 ) correspond to 16 and 21 mg/kg dw MES using the most sensitive endpoint, chick mortality. Both of these values are higher than the 6 mg/kg dw level proposed by Skorupa (1998) who based his estimate on field-observational data potentially confounded by other environmental stress factors. The mortality and teratogenicity endpoints presented here relate selenium exposure to risk to individuals within a population and do not provide information about the probability of selenium causing changes in population growth rates, either at the local or regional levels.

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“…Early studies have shown that Se from plants added to the diet in excess of 4 ppm can impair reproductive success and is teratogenic to chickens (Poley and Moxon, 1938). The biological role of Se was first associated with antioxidant activity (Schwarz and Foltz, 1957), then with enzymatic activity of glutathione peroxidase (Rotruck et al, 1973) and more recently as an essential nutrient (Levander, 1986).…”

Section: Introductionmentioning

confidence: 99%

Subchronic hepatotoxicity of selenomethionine ingestion in mallard ducks

Hoffman

Heinz

LeCaptain

et al. 1991

Journal of Toxicology and Environmental Health

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Two-year-old male mallards (Anas platyrhynchos) received a control diet (0.2 ppm Se) or diets containing 1, 2, 4, 8, 16, or 32 ppm Se as selenomethionine for 14 wk. Se accumulated readily in the liver in a dose-dependent manner, reaching a mean concentration of 29 ppm (wet weight) in the 32 ppm group. Dietary Se of 2 ppm or greater increased plasma glutathione peroxidase activity. Mortality (10%) and histopathological effects, including bile duct hyperplasia and hemosiderin pigmentation of the liver and spleen, occurred in the 32 ppm group. These histopathological effects were accompanied by lower hemoglobin concentrations (16 and 32 ppm groups) and hematocrit (32 ppm group), and elevated plasma alkaline phosphatase activity (32 ppm group) indicative of cholestatic liver injury. Other manifestations of hepatotoxicity included significant linear dose responses for hepatic oxidized glutathione (GSSG) concentrations and ratio of GSSG to reduced glutathione (GSH). Means for both of these responses differed from controls in groups receiving 8-32 ppm Se. Mean hepatic GSH and malondialdehyde (a measure of lipid peroxidation) concentrations were significantly elevated in the 16 and 32 ppm groups. Subchronic effects of selenomethionine, which occurs in vegetation, are of particular interest with respect to the health of wild aquatic birds in seleniferous locations.

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Tolerance Levels of Seleniferous Grains in Laying Rations

Cited by 39 publications

References 3 publications

Embryotoxic and teratogenic effects of selenium in the diet of mallards

Embryotoxic and teratogenic effects of selenium in the diet of mallards

Egg Selenium Concentrations as Predictors of Avian Toxicity

Subchronic hepatotoxicity of selenomethionine ingestion in mallard ducks

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