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Selenium toxicity: cause and effects in aquatic birds.

Publication ,  Journal Article
Spallholz, JE; Hoffman, DJ
Published in: Aquatic toxicology (Amsterdam, Netherlands)
April 2002

There are several manners in which selenium may express its toxicity: (1) an important mechanism appears to involve the formation of CH(3)Se(minus sign) 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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Published In

Aquatic toxicology (Amsterdam, Netherlands)

DOI

EISSN

1879-1514

ISSN

0166-445X

Publication Date

April 2002

Volume

57

Issue

1-2

Start / End Page

27 / 37

Related Subject Headings

  • Toxicology
  • Selenomethionine
  • Selenium
  • Oxidation-Reduction
  • Liver
  • Ducks
  • Birds
  • Antioxidants
  • Animals
  • 41 Environmental sciences
 

Citation

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Spallholz, J. E., & Hoffman, D. J. (2002). Selenium toxicity: cause and effects in aquatic birds. Aquatic Toxicology (Amsterdam, Netherlands), 57(1–2), 27–37. https://doi.org/10.1016/s0166-445x(01)00268-5
Spallholz, Julian E., and David J. Hoffman. “Selenium toxicity: cause and effects in aquatic birds.Aquatic Toxicology (Amsterdam, Netherlands) 57, no. 1–2 (April 2002): 27–37. https://doi.org/10.1016/s0166-445x(01)00268-5.
Spallholz JE, Hoffman DJ. Selenium toxicity: cause and effects in aquatic birds. Aquatic toxicology (Amsterdam, Netherlands). 2002 Apr;57(1–2):27–37.
Spallholz, Julian E., and David J. Hoffman. “Selenium toxicity: cause and effects in aquatic birds.Aquatic Toxicology (Amsterdam, Netherlands), vol. 57, no. 1–2, Apr. 2002, pp. 27–37. Epmc, doi:10.1016/s0166-445x(01)00268-5.
Spallholz JE, Hoffman DJ. Selenium toxicity: cause and effects in aquatic birds. Aquatic toxicology (Amsterdam, Netherlands). 2002 Apr;57(1–2):27–37.
Journal cover image

Published In

Aquatic toxicology (Amsterdam, Netherlands)

DOI

EISSN

1879-1514

ISSN

0166-445X

Publication Date

April 2002

Volume

57

Issue

1-2

Start / End Page

27 / 37

Related Subject Headings

  • Toxicology
  • Selenomethionine
  • Selenium
  • Oxidation-Reduction
  • Liver
  • Ducks
  • Birds
  • Antioxidants
  • Animals
  • 41 Environmental sciences