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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

Studies on the mechanism of selenium poisoning in the animal body

Klug, Harlan Lyle, January 1949 (has links)
Thesis (Ph. D.)--University of Wisconsin--Madison, 1949. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 122-133).
2

Acute and chronic effects of selenium on D̲a̲p̲h̲n̲i̲a̲ p̲u̲l̲e̲x̲ /

Reading, Jeffrey Thomas, January 1979 (has links)
Thesis (M.S.)--Virginia Polytechnic Institute and State University. / Vita. Abstract. Includes bibliographical references (leaves 72-82). Also available via the Internet.
3

Evaluation of selenium toxicity on cellular metabolism : effects of selenite and selenomethionine /

Toy-Manning, Pamela Ann January 1980 (has links)
No description available.
4

Acute and chronic effects of selenium on Daphnia pulex

Reading, Jeffrey Thomas 23 February 2010 (has links)
Acute toxicity tests with selenium were conducted with three freshwater species. All data are expressed as selenite-selenium. Daphnia pulex had a 48 hr LC50 of 3.87 mg/l selenium. The 96 hr LC50 and EC50O values for Gambusia affinis and Physa sp. respectively, were 12.56 and 27.08 mg/l selenium. The sublethal effects of 0.2, 0.4, 0.6 and 0.8 mg/1 selenium on survival, growth and reproduction of Daphnia pulex were monitored for twenty-eight days. These results were analyzed statistically by brood. Appreciable mortality only occurred at 0.8 mg/l selenium. Growth, as measured by body length, was depressed at the highest concentration during the early instars and was slightly stimulated during the later instars. Number of live young per brood was depressed at 0.4, 0.6 and 0.8 mg/l selenium during the early broods and may have been stimulated in later broods. Reproductive dysfunction (i.e., dead young, deteriorated eggs, and abortions) only was significant at the higher concentrations in the early broods. It appeared that the Daphnia were acclimating to the selenium stress. Based on these studies, the MATC for selenite-selenium was 280 ug/l. The effects of selenium on oxygen consumption and filtering rate during 24 hr exposure were also tested at the above concentrations. There were no significant effects of selenium on oxygen consumption. Selenium slightly stimulated filtering rate at 0.2 mg/l and depressed it at the higher concentrations. An evaluation of the water quality criteria for selenium in fresh water indicates that all of the methods for deriving these proposed criteria are inadequate. Based on my evaluation a dual criterion seems appropriate: a strict criterion for selenate-selenium and lenient criterion for selenite- and biselenite-selenium. / Master of Science
5

Effect of dietary fluoride on selenite toxicity in the rat

Yu, Qing, 1966- 28 January 1992 (has links)
Two factorial experiments were conducted to determine if high dietary fluoride would inhibit selenite toxicity in rats. In each study, two levels of selenite (0.05 and 5 mg/kg diet) were matched against two levels of fluoride (1 and 150 mg/kg diet) for either 6 or 8 weeks. Fluoride failed to prevent the depressive effect of selenite on food intake and body weight gain in either study. Although liver selenium concentration was slightly (15%) but significantly (P < 0.005) reduced when the highest fluoride and selenium level were combined in the first study, this effect could not be repeated. These three measures therefore failed to provide evidence for a fluoride and selenium interaction. Fluoride, however, prevented hepatic necrosis seen in most of the selenite-toxic rats. Hepatic lesions seen histologically in selenite-toxic rats were not observed for either kidney or heart. With regard to a possible mechanism for the fluoride effect upon selenite liver pathology, fluoride partially (26%) but significantly (P < 0.025) reduced thiobarbituricreactive substances (an indicator of peroxidative cell membrane damage) in selenite-toxic rats, but there was no fluoride effect on an enzyme system (liver xanthine oxidase) that potentially could generate an initiator of lipid peroxidation. In agreement with results of others, fluoride deposition into bone was inconsistently affected by selenite, Overall, the protective effect of fluoride on selenite toxicity appears to be confined to liver pathology. The exact mechanism for this effect, however, remains unclear. / Graduation date: 1992
6

The effect of lead and zinc on selenium poisoning in mice

Call, Cynthia Joy 01 August 1975 (has links)
Trace elements, because they are effective in catalytic amounts, must be held in delicate balance with each other as well as with the macronutrients of the diet. Disturbances of these balances result in deficiency and toxicity symptoms. Toxic doses of selenium, lead, and zinc, for example, are known to cause anemia (1, 2, 3, 4) and growth depression (5, 3) in experimental animals.
7

Post-hatching survival and productivity of American avocets at drainwater evaporation ponds in the Tulare Basin, California

Marn, Carolyn M. (Carolyn Mary), 1962- 29 April 2003 (has links)
Evaporation ponds that dispose of agricultural drainwater provide attractive habitat for waterbirds but may result in contaminant exposure that impairs reproduction. I estimated post-hatching survival and evaluated productivity estimates for American avocets (Recurvirostra americana) nesting at evaporation ponds in the Tulare Basin, California from 1991 to 1993. Avocets and Black-necked stilts (Himantopus mexicanus) comprised the majority of 5,969 nests found. Nest success and embryo mortality varied among ponds and between species. Embryo deformity and mortality rates associated with selenium were higher in stilts. The majority of reproductive losses were attributed to predation, especially at ponds without islands. Post-hatch survival of radiomarked avocets after 5 weeks ranged from 0.375-0.729 and differed among ponds (log-rank X²=7.12, 2 df, P=0.028). Predation accounted for 55.4% (36/65) of known mortalities. Depredated chicks ranged from 1-30 days of age with a median age of 6 days. Arsenic concentrations in avocet livers were below detection limits while boron concentrations were below detection limits at Westlake-South (WLS) and Tulare Lake Drainage District-South (TLDD-S) in 1993. Mean boron concentration in livers was 3.7 ppm at TLDD-S in 1992 and 22.9 ppm at Lost Hills Water District (LHWD). Liver selenium concentrations increased with age and differed among ponds (P=0.0001). Mercury concentrations differed among ponds (P=0.0001), but were similar to background. Growth, survival and selenium exposure were consistent to support post-hatching effects of selenium. Mortality in avocet chicks was highest at LHWD, intermediate at TLDD-S and lowest at WLS, consistent with selenium exposures. I observed lower survival, histologic lesions, lower hatchling weights, slower growth, and elevated selenium and boron in tissue at LHWD. I used capture-recapture analysis also to estimate post-hatching survival and calculated avocet productivity. Survival estimates for the first 4 weeks post-hatching, based on model averaging, ranged from 0.572 to 0.751. Productivity at some ponds was insufficient to offset adult mortality. Estimates of average annual productivity were 0.49 and 0.45 in 1992 and 1993, respectively. Juvenile survival rates necessary for recruitment to offset 10% and 20% adult mortality ranged from 0.204 to 0.408 and 0.222 to 0.444, respectively. / Graduation date: 2004

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