Selenium toxicity: cause and effects in aquatic birds

Abstract

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.

Selenium bioaccumulation and speciation in Chironomus dilutus exposed to water‐borne selenate, selenite, or seleno‐DL‐methionine

“…The predominance of organic selenides (R-Se-R; modeled as selenomethionine) in larvae from the selenite treatment was surprising. Animals have no mechanism for the synthesis of the amino acid methionine and consequently are unable to synthesize Se-met; instead, animals obtain methionine and Se-met primarily from their diet [13]. Bacterial reduction of selenite to organic selenides is postulated as the most likely mechanism whereby larvae from the selenite treatment accumulated elevated concentrations of organic selenides.…”

“…Biotransformation of Se and the incorporation of organoselenium compounds into proteins are key steps in the trophic transfer of Se [11]. Aquatic insects can biotransform inorganic Se into organic forms [12], which are the predominant forms of Se ingested by birds and fish [13]. In particular, selenomethionine has been shown to cause embryonic deformities, other teratogenic effects, and mortality of bird embryos at dietary concentrations as low as 8 mg/g wet weight [14].…”

Detection of metals in proteins by means of polyacrylamide gel electrophoresis and laser ablation‐inductively coupled plasma‐mass spectrometry: Application to selenium

“…Next to acute Se poisoning, selenosis, various toxic effects of Se have been reported, such as teratogenic effects on embryonic development, especially in wildlife [7,8]. These selonoproteins or Se-containing proteins are efficiently fractionated by gel electrophoresis.…”

Effect of foliar application of selenium on the content of selected amino acids in potato tubers (Solanum tuberosum L.)

“…There are several ways in which selenium may express its toxicity (Spallholz and Hoffman 2002). The selenium present in plants that are resistant to high rates of Se is a component of non-protein amino acids (Whanger 2002).…”