There are several manners in which selenium may express its toxicity: (1) an important mechanism appears to involve the formation of CH3Se- 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.