Toxicity of Various Selenium Derivatives to Chick Embryos

Palmer, I. S.; Arnold, R. L.; Carlson, C. W.

doi:10.3382/ps.0521841

Cited by 46 publications

(22 citation statements)

References 10 publications

(7 reference statements)

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“…Similar studies were done by Halverson et al (1965). The most interesting of these kinds of experiments were done by Palmer et al (1973). They investigated the toxicity of eight different selenium compounds by direct injection of increasing concentrations of selenium into 4-day-old embryos.…”

Section: Egg Injection Studies With Selenium Compoundsmentioning

confidence: 78%

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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Section: Egg Injection Studies With Selenium Compoundsmentioning

confidence: 78%

Selenium toxicity: cause and effects in aquatic birds

Spallholz

Hoffman²

2002

Aquatic Toxicology

214

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“…However, egg injections of sodium selenite were reported to cause malformations similar to those caused by selenomethionine (summarized by Olson, 1986), which also included thinning of the ventricular walls of the heart (Khan and Gilani, 1980), as well as gastroschisis (Sukra et al, 1976). Selenomethionine is also an effective teratogen when injected into the air cell of chicken eggs (Palmer et al, 1973). Selenomethionine has been reported to be the major form of selenium in certain plants including wheat (Allaway et al, 1967;Olson, 1986), and therefore may have been present in plants consumed by aquatic birds at Kesterson NWR.…”

Section: Discussionmentioning

confidence: 96%

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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“…In birds, selenium-caused malformations, such as hydrocephaly, beak defects, microphthalmia, anophthalmia, and foot defects, were observed in duck [2,3] and chicken [4][5][6] embryos when given to hens or injected to eggs. In mammals, however, teratogenicity of Se has not been clearly shown.…”

Section: Introductionmentioning

confidence: 99%

“…The observed malformations, such as deformed optic vesicle and swollen rhombencephalon, were considered to correspond to microphthalmia, encephalocele, observed in hamster fetuses at maternotoxic dose of Se [8] and in bird embryos treated with Se by egg injection or feeding to hens [3,4]. It is therefore considered that cultured rat embryos provide a model for the investigation into Se teratogenicity.…”

Section: Introductionmentioning

confidence: 99%