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A Conceptual Framework Describing Mercury Bioavailability to Microbes Through Redox ZonesStenzler, Benjamin 01 June 2022 (has links)
Mercury (Hg) is a global pollutant and potent neurotoxin that is detrimental to the environment and human health. (MeHg). All forms of Hg are toxic, but methylmercury (MeHg) can biomagnify through food webs and become concentrated in food staples such as fish and rice, creating an exposure risk to people. The conversion of Hg to MeHg is mediated by anaerobic microbes, particularly sulfate and iron-reducing bacteria and methanogenic archaea. However, Hg methylation is an intracellular process, and MeHg production is dependent on the bioavailability of inorganic Hg to these microbes. One outstanding knowledge gap in understanding Hg methylation is the nature of bioavailability of inorganic divalent Hg (HgII). Much research has gone into developing a framework describing how microbes take up Hg for methylation. Still, the framework describing Hg bioavailability processes is not fully developed. The overall objective of my thesis is to address these mechanisms governing HgII bioavailability to anaerobic microbes.
HgII bioavailability is determined by its speciation; these are all the different forms and compounds of HgII. To address the bioavailability of various HgII species, I used microbial Hg-biosensors. Hg-biosensors are bacterial cells that emit a quantifiable signal when HgII enters them and let me observe HgII bioavailability in real-time. The biosensors I developed are the first Hg-biosensors that function without oxygen and let me explore HgII species and their bioavailability under conditions conducive to methylation. HgII speciation is spatially and temporally dynamic moving from oxic to anoxic conditions and under various biogeochemical controls. I follow HgII speciation and bioavailability in my thesis as it transgresses through these conditions. Understanding HgII bioavailability to complex microbial communities across redox gradients and through dynamic ligand interactions is a missing key component to understanding and predicting MeHg formation.
My results show how altering HgII speciation can identify novel bioavailability pathways or make it completely inaccessible. My results highlight how microbes can control HgII bioavailability and the importance of microbial community structure on metal acquisition. First, I resolve pathways for charged inorganic HgII species through the cell membrane and demonstrate novel pathways for previously unconsidered charged species. Using dissolved organic matter (DOM) originating from various algal species, I show how algae can uniquely control HgII bioavailability to other organisms. I demonstrate how DOM has emergent properties that can control HgII bioavailability. Next, I investigated the compounds microbes use to scavenge metals such as iron and copper. I reveal how they could inadvertently interact with HgII and form new bioavailability pathways. Lastly, I demonstrate how the diffusion of biogenic hydrogen sulfide from an isolated system can make an otherwise non-bioavailable HgII species rapidly available for microbial uptake. Overall, my thesis expands the framework describing HgII bioavailability to microbes and potential drivers of Hg methylation in the environment.
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Variation in Habitat Use and its Consequences for Mercury Exposure in Eastern Ontario Bats (Myotis lucifugus and Eptesicus fuscus)Bedard, Bailey 03 March 2022 (has links)
Insectivorous bats have been found to have unusually high levels of mercury. While broad geographic scale studies have investigated factors contributing to mercury bioaccumulation in bats across Canada, studies investigating differences in regional scale bioaccumulation and the contributing factors remain scarce. Here, I comprehensively investigate the bioaccumulation of mercury in two insectivorous bats, the big brown bat (Eptesicus fuscus) and the little brown bat (Myotis lucifugus), collected over a period of ~20 years along the St. Lawrence River in Eastern Ontario, parts of which are historical hotspots of mercury, to address two objectives: First the determination of biological and environmental factors, including dietary sources, contributing to reported patterns of fur total mercury bioaccumulation, and second the investigation of DNA-based biomarkers as potential tools to assess internal tissue-responsiveness to mercury exposure, specifically global DNA methylation and expression levels of mitochondrial DNA. With regard to factors determining fur total mercury concentration in Eastern Ontario bats, significant differences between species exist, as higher concentrations were found in big brown bats compared to little brown bats. Sex contributed to differences in fur total mercury, however in a species-specific manner. Male fur contained higher total mercury concentrations compared to females in big brown bats, but not little brown bats. Female reproductive status differentially affected fur mercury concentrations between both species, reducing concentrations in pregnant little brown bats, while significantly increasing concentrations during lactation in big brown bats. Finally, fur total mercury concentration in adults was higher than that of juvenile bats (< 1 yr). To address the hypothesis that aquatic emerging and terrestrial insect diets differentially contribute to Eastern Ontario bat mercury concentration, I used stable isotope analysis and telemetry approaches and caught aquatic and terrestrial insects. While higher total mercury was identified in aquatic compared to terrestrial insects, a high degree of variability in the isotope signature in insects and bats in Eastern Ontario did not allow to fully address this hypothesis. However, data pointed to a more specialized diet in big brown bats compared to a more generalist diet in little brown bats as well as a sex-specific correlation between dietary source and fur total mercury concentration in little and big brown bats. The evaluation of potential epigenetic and mitochondrial DNA-level molecular biomarkers in kidney, brain and liver (DNA methylation and assessment of relative mitochondrial DNA copy number) did not reveal significant correlations with fur total mercury concentrations. This may suggest that the mercury concentrations measured in this study were not high enough to elicit these specific DNA level responses or they do not represent relevant biomarkers of environmental methylmercury exposure, at least in big brown bats. Overall, this thesis contributes to our understanding of regional variability in fur total mercury concentration within and between Eastern Ontario bat species. These findings provide important insights for future targeted investigations of the contribution of aquatic emerging and terrestrial insect dietary sources on the one hand and underline the importance of accounting for regional variability in more global scale comparisons of bat mercury bioaccumulation on the other.
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Condensation of metal vapors : mercury and the kinetic theory of condensation /Wilhelm, Donald James January 1964 (has links)
No description available.
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The stability and nature of complexes of mercury with higher phosphates /Simonaitis, Richard Ambrose January 1962 (has links)
No description available.
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Directional correlations between X rays and internal conversion electrons in samarium 145, gold 195, and mercury 203.Brannan, John Robert January 1969 (has links)
No description available.
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Complexes of mercury(I) and iron(III) with polyphosphates /Memon, Ali Nawaz January 1972 (has links)
No description available.
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The use of cladophora to monitor mercury occurrence in western Lake Erie waters /Burkett, Robert Dale January 1973 (has links)
No description available.
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The solubility of mercury in polar gases /Rosenberg, Harvey Sanford January 1973 (has links)
No description available.
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Tim-3 and Cell Death in Murine Mercury Induced AutoimmunitySchiraldi, Michael January 2011 (has links)
There is a role for environmental factors in the pathogenesis of autoimmune diseases in humans and animals. Correlations have been made between mercury (Hg) exposure and the prevalence human autoimmune diseases. The rodent model of Hg-induced autoimmunity is useful for the analysis of systemic autoimmunity that is both environmentally and genetically modulated. In susceptible mice, Hg treatment induces both polyclonal activation of B cells, as well as the production of highly specific autoantibodies targeting the nucleolar protein fibrillarin. Tim proteins are a family of immune cell surface molecules that have been implicated in modulation of autoimmune diseases in both humans and animals. Tim-3, originally reported as a Th1 specific molecule, is expressed on T cells of various subsets, as well as antigen presenting cells and granulocytes. Tim-3 and its known ligand galectin-9 play a role in the down-regulation of immune responses, including experimental autoimmune encephalomyelitis and autoimmune conjunctivitis. Tim-3-Ig fusion protein, as well as blocking and stimulating anti-Tim-3 antibodies, were employed in vivo to modulate the Tim-3-galectin-9 pathway during Hg-induced autoimmunity. Results have shown an increase in Th1 manifestations and decrease in Th2 manifestations when the pathway is inhibited by Tim-3-Ig. Blockade of the pathway using a Tim-3 directed antibody resulted in an increase of all disease manifestations, including Th2-driven IgE production; a stimulating antibody had the opposite effect on IgG and no effect on IgE. In addition to studying the regulation of Hg-induced autoimmunity, a goal of immunologists is to understand the genesis of this disease model. Apoptosis, although anti-inflammatory, has been proposed as a source of autoantigen in autoimmune diseases. Interest in events occurring at the site of Hg injection has prompted us to perform in vitro studies of Hg-induced cell death. Treatment of murine lung epithelial cells or Jurkat T cells with doses of Hg similar to those present at the injection site results in a death process that is morphologically and biochemically distinct from apoptosis. We have observed peripheral movement of the nucleolar protein fibrillarin via confocal microscopic study of Hg-induced cell death. As cells die, there is extrusion of fibrillarin from the nucleus and exposure at the cell surface. Such cell death may allow recognition of fibrillarin by the immune system thereby promoting the formation of anti-nucleolar antibodies. / Microbiology and Immunology
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A Mechanistic Model to Examine Mercury in Aquatic SystemsHarris, Reed 03 1900 (has links)
Elevated mercury levels have been observed in a wide variety of aquatic systems. A mass balance non-steady state model was developed to examine mercury cycling in lakes and reservoirs. Hg(ll), methylmercury, Hg° , dimethylmercury and solid phase HgS cycles were interconnected. Compartments included air, water, sediment, suspended solids, plankton, benthos, and two generic fish categories based on diet. Bioenergetics equations for individual fish were extended to consider mercury dynamics for entire fish populations. Biota represented large methylmercury fluxes in the water column and were found to be important methylmercury repositories. In a simulation of a generic well-mixed shield lake in Ontario, the fish population contained about 4 times as much methylmercury as water. Uptake of methylmercury by individual walleye and yellow perch was predicted to be dominated by the food pathway (eg. 99% of total uptake).
Based on simulations for the generic shield lake, the watershed has the potential to be an important source of methylmercury in some shield lakes (exceeding in-situ methylation in the generic simulation). Methylation in the water column and sediments were both simulated to be significant. Simulated net production of methylmercury in the generic shield lake was on the order of 0.05 to 0.15 ug methylmercury m⁻² year⁻¹ in the water column, with similar rates in sediments. Simulated rates of net methylation in polluted sytems were higher. Fractions of total dissolved Hg(II) or methylmercury available for methylation and demethylation in aerobic waters were thermodynamically predicted to be small (e.g. <1%). Dissolved organic carbon and sulphides (if present) were thermodynamically predicted to dominate Hg(II) and methylmercury complexation in freshwaters. Hg(II) burial and outflows represented about 85-90% of total mercury losses for the generic shield lake (2 year hydraulic retention time). Volatilization of Hg° , produced by demethylation and Hg(II) reduction, represented the remaining 10-15% of losses. Considerable system to system variability is expected for sources and sinks of total mercury and methylmercury in shield lakes. In simulations of two mercury contaminated environments, Lake St. Clair and Clay Lake, Ontario, sediment return of Hg(II) caused the lakes to be net sources of mercury to downstream areas. Sediment return of mercury could partially explain observed two-phase recoveries of fish methylmercury levels in some polluted systems. The time required for Hg(II) and methylmercury concentrations in various compartments to respond to changes in loads was simulated. There was a tendency towards relatively rapid internal cycling of Hg(II) and methylmercury, but slower overall system response times (eg. years to decades to respond to recover from flooding or pollution episodes). / Thesis / Master of Engineering (ME)
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