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Lyn G. Gold

Publications and source records attributed to Lyn G. Gold.

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Selenium accumulation and elimination in mallards

Selenium accumulation and loss were measured in adult mallards ( Anas platyrhynchos ) fed selenomethionine during two experiments. In Experiment 1, both sexes were fed a diet containing 10 ppm selenium for 6 weeks, followed by 6 weeks on untreated feed. Selenium accumulation in liver and muscle of females was described by C=A(1−e −bt ). Concentrations of selenium were predicted to reach 95% of equilibrium faster in liver (7.8 days) than in muscle (81 days). The loss of selenium from liver and muscle of females was described by the exponential loss rate equation: C=Ae −bt , with half-times of 18.7 and 30.1 days, respectively. Males reached similar levels of selenium in liver and breast muscle as females and declined to similar levels once selenium treatment ended. In Experiment 2, females were fed increasing levels of selenium until some died. Survivors were switched to an untreated diet and selenium was measured in blood, liver, and breast muscle over 64 days. The same equation as in Experiment 1, C=Ae −bt , was used to describe the loss of selenium from blood and muscle. Halftimes were 9.8 and 23.9 days, respectively. For liver, the equation C C = A 1 e − b 1 t + A 2 e − b 2 t "> = A 1 e −b 1 t + A 2 e −b 2 t was used. Selenium initially decreased in liver by one-half in 3.3 days, with subsequent half-times of 3.9, 6.0, and 45.1 days.

Archives of Environmental Contamination and Toxico

Impaired reproduction of mallards fed an organic form of selenium

We fed mallards ( Anas platyrhynchos ) diets supplemented with 0-, 1-, 2-, 4-, 8-, or 16-ppm selenium in the form of selenomethionine. We fed another group of mallards a diet containing 16-ppm selenium as selenocystine. Females fed the control diet produced a mean of 8.1 ducklings that survived to 6 days of age, which was significantly greater than the 4.6 young produced by females fed 8-ppm selenium as selenomethionine and the zero surviving young of females fed 16-ppm selenium as selenomethionine. Selenocystine did not impair reproduction. Diets containing 8- and 16-ppm selenium as selenomethionine caused malformations in 6.8 and 67.9%, respectively, of unhatched eggs compared with 0.6% for controls. The most common malformations were of eyes, bill, legs, and feet. Selenium did not affect the onset or frequency of egg laying, egg size, shell thickness, fertility of eggs, or sex ratio of ducklings. Reduced survival and growth occurred in ducklings hatched from groups whose parents had received 8- or 16-ppm selenium as selenomethionine, even though all ducklings were fed a control diet. Concentrations of selenium in eggs and liver of adults could be predicted from dietary concentrations. We conclude that the dietary threshold of selenium as selenomethionine necessary to impair reproduction is between 4 and 8 ppm. It is difficult to identify 1 level of selenium in eggs that will be diagnostic of reproductive impairment in the field because different chemical forms of selenium appear to have different toxicities in eggs. However, when eggs from a wild population contain .gtoreq. 1-ppm selenium on a wet-weight basis, reproductive impairment may be possible and should be evaluated in that population. At 5-ppm selenium in eggs, reproductive impairment is much more likely to occur.

Journal of Wildlife Management

Toxicity of organic and inorganic selenium to mallard ducklings

The toxicity of selenomethionine and sodium selenite to mallard ducklings ( Anas platyrhynchos ) was measured by feeding each form from hatching to six weeks of age at dietary concentrations of 0, 10, 20, 40, and 80 ppm selenium. At 80 ppm selenium, sodium selenite caused 97.5% mortality by six weeks and selenomethionine caused 100% mortality. At 40 ppm, these two forms of selenium caused 25 and 12.5% mortality. No mortality occurred at 10 or 20 ppm. Diets containing 20, 40, or 80 ppm selenium in both forms caused decreases in food consumption and growth. The only statistically significant effect of 10 ppm selenium was with sodium selenite, which resulted in larger livers than controls. Selenomethionine was more readily stored in the liver than sodium selenite at levels above 10 ppm selenium in the diet. Based on comparisons of residues of selenium in livers of surviving and dead ducklings, concentrations in the liver were not diagnostic of death due to selenium poisoning. Because both forms of selenium resulted in severe reductions in food consumption, selenium-induced starvation may have been related to duckling mortality. It was not clear whether either form of selenium at 10 ppm in the diet resulted in a leveling off of selenium concentrations in the liver within six weeks.

Archives of Environmental Contamination and Toxico

Behavior of mallard ducklings from adults exposed to selenium

Pairs of adult mallards ( Anas platyrhynchos ) were fed a control diet or a diet containing 1, 2, 4 or 8 ppm selenium in the form of seleno-DL-methionine. Ducklings from these pairs were fed an untreated diet from hatching through 6 d of age, at which time their avoidance of a fright stimulus was tested. Selenium had no effect on the ducklings' response to the fright stimulus.

Environmental Toxicology and Chemistry