Embryotoxic and teratogenic effects of selenium in the diet of mallards

Hoffman, David J.; Heinz, Gary H.

doi:10.1080/15287398809531178

Cited by 116 publications

(67 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Se 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 with controls (Heinz et al, 1987;Hoffman and Heinz, 1988). About 10 ppm Se as selenomethionine was more teratogenic than sodium selenite at 25 ppm.…”

Section: Reproducti6e Effectsmentioning

confidence: 91%

Selenium toxicity: cause and effects in aquatic birds

Spallholz

Hoffman²

2002

Aquatic Toxicology

216

View full text Add to dashboard Cite

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.

show abstract

Section: Reproducti6e Effectsmentioning

confidence: 91%

Selenium toxicity: cause and effects in aquatic birds

Spallholz

Hoffman²

2002

Aquatic Toxicology

216

View full text Add to dashboard Cite

show abstract

“…A potential candidate based on the mammalian literature is glutathione peroxidase (GPx) activity and/or the cellular levels of reduced glutathione and hydrogen selenide (Greeley, M.S., Oak Ridge National Laboratory, personal communication, Jan. 22, 1999). Evidence of increased lipid peroxidation and related glutathione peroxidase activity has been found in aquatic birds at sites such as Kesterson (Hoffman and Heinz 1988;Ohlendorf et al 1988). Selenium has an antimutagenic effect so genomic research is not feasible.…”

Section: Executive Summarymentioning

confidence: 99%

“…As with fish, however, much is unknown regarding uptake and specific transformations within the various species. For example, Hoffman and Heinz (1988) report that the mode of action of embryotoxicity and teratogenesis of selenium on mallards is uncertain. Evidence of increased lipid peroxidation and related glutathione peroxidase activity were found by Hoffman and Heinz (1988) and in coots from Kesterson by Ohlendorf et al (1988).…”

Section: Toxicity To Birdsmentioning

confidence: 99%

“…For example, Hoffman and Heinz (1988) report that the mode of action of embryotoxicity and teratogenesis of selenium on mallards is uncertain. Evidence of increased lipid peroxidation and related glutathione peroxidase activity were found by Hoffman and Heinz (1988) and in coots from Kesterson by Ohlendorf et al (1988). Selenium-caused oxidant-induced stress or damage and increased lipid peroxidation has been identified in mammals (Dougherty and Hoekstra 1982), and increases in organic solventsoluble lipofuchsin pigments of the liver as well as glutathione peroxidase activity were identified in mice (Csallany et al1984).…”

Section: Toxicity To Birdsmentioning

confidence: 99%

See 1 more Smart Citation

Selenium Poisoning of Wildlife and Western Agriculture: Cause and Effect

Korte

2000

View full text Add to dashboard Cite

“…Selenium is both embryotoxic and teratogenic to birds, with organic selenium (selenomethionine) being more toxic than inorgipic selenium (Hoffman and Heinz, 1988). Mallard ducks were fed diets containing 1, 5, 10,25, or 100 ppm selenite (Heinz et al, 1987) or 1, 2, 4, 8, or 16 ppm selenomethionine (Heinz et al, 1989) for about 10 weeks.…”

Section: )mentioning

confidence: 99%

Preliminary assessment of the ecological risks to wide-ranging wildlife species on the Oak Ridge Reservation

Sample¹,

Baron²,

Jackson³

1995

View full text Add to dashboard Cite

DlSTRlBUTlON OF Q S T IThis report has been reproduced directly from the best available copy.Available to DOE DISCLAIMERThis report was prepared as an account of work sponsored by an agency of the United States Government. Neither the United States Government nor any agency thereof, nor any of their employees, make any warranty, express or implied, or assumes any legal liability or responsibility for the accuracy, completeness, or usefulness of any information, apparatus, product, or process disclosed, or represents that its use would not infringe privately owned rights. Reference herein t o any specific commercial product, process, or service by trade name, trademark, manufacturer, or otherwise does not necessarily constitute or imply its endorsement, recommendation, or favoring by the United States Government or any agency thereof. The views and opinions of authors expressed herein do not necessarily state or reflect those of the United States Government or any agency thereof. DISCLAIMER 2-2 G-40Soil-plant uptake factors fiom collocated soil and plant samples collected G-52Soil-plant organic contaminant uptake factors using octanol water F-18HQs for contaminants of potential concern for white-tailed deer on the ORR ..... ACKNOWLEDGMENTSThis report is the result of the efforts, contributions, and support of many persons. We are grateful to Sigurd Christensen, Craig Brandt, Michelle Bell, and John Fackenthal for their work in identi%@, locating, and acquiring data for use in this assessment. We also thank all of the ER personnel who responded to requests for data and provided input and support. We thank the following for providing us with their data and aiding in it's interpretation: George Southworth, Mark Peterson, Walter Hill, Rich Stevens, Chuck Hadden, Pat Ryon, Christy Anderson, Robert Brewer, Dick Halbrook, Chris Welsh, and Jim Evans. Brent Ziegler and John Paul Van Stone provided technical support. All maps were produced by Robert Washington-Allen. Finally, this report has benefitted from the reviews of Glenn Suter and Tom Ashwood. xv i EXECUTIVE SUMMARYHistorically, ecological risk assessment at CERCLA sites [such as the Oak Ridge Reservation (OW)], has focused on species that may be definitively associated with a Contaminated area or source operable unit. This is necessary to identify areas where risk is sufficiently high to warrant remediation. Consequently the species that are generally considered are those with home ranges small enough such that multiple individuals or a distinct population can be expected to reside within the boundaries of the contaminated site. This approach is adequate for sites with single, discrete areas of contamination that only provide habitat for species with limited spatial (e.g., small home range) requirements. This approach is not adequate however for large sites with multiple, spatially separated contaminated areas that provide habitat for wide-ranging wildlife species. Because wide-ranging wildlife species may travel between and use multiple contaminate...

show abstract

Embryotoxic and teratogenic effects of selenium in the diet of mallards

Cited by 116 publications

References 29 publications

Selenium toxicity: cause and effects in aquatic birds

Selenium toxicity: cause and effects in aquatic birds

Selenium Poisoning of Wildlife and Western Agriculture: Cause and Effect

Preliminary assessment of the ecological risks to wide-ranging wildlife species on the Oak Ridge Reservation

Contact Info

Product

Resources

About