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Dissertations / Theses on the topic 'Methylmercury'

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Published: 4 June 2021

Last updated: 26 February 2023

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1

Tanner, Kari Christine. "Methylmercury in California Rice Ecosystems." Thesis, University of California, Davis, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10642100.

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Methylmercury (MeHg) is a toxic and bioaccumulative form of mercury that can be produced by bacteria living in water saturated soils, including those found in flooded rice fields. In the Sacramento Valley, California, rice is grown on 240,000 hectares, and mercury is a concern due to a history of mining in the surrounding mountains.

Using unfiltered aqueous MeHg data from MeHg monitoring programs in the Sacramento River watershed from 1996 to 2007, the MeHg contribution from rice systems to the Sacramento River, was assessed. AgDrain MeHg concentrations were elevated compared to upstream river water during November through May, but were not significantly different during June through October. June through October AgDrain MeHg loads (concentration × flow) contributed 10.7–14.8% of the total Sacramento River MeHg load. Missing flow data prevented calculation of the percent contribution of AgDrains in November through May.

Field scale MeHg dynamics were studied in two commercial rice fields in the Sacramento Valley. The Studied fields had soil total mercury concentrations of 25 and 57 ng g^-1, which is near the global background level. Surface water and rice grain MeHg and THg concentrations were low compared to previously studied fields. An analysis of surface water drainage loads indicates that both fields were net MeHg importers during the growing season and net MeHg exporters during the fallow season.

Since the microbes that produce MeHg prefer flooded environments, management that dries the soil might reduce MeHg production. Conventional continuously flooded (CF) rice field water management was compared to alternate wetting and drying, where irrigation was stopped twice during the growing season, allowing soil to dry to 35% volumetric moisture content, at which point plots were re-flooded (AWD-35). Compared to CF, AWD-35 resulted in a significant reduction of MeHg concentration in soil, surface water and rice grain.

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2

Campbell, Sonja Gray. "Methylmercury Neurotoxicity and Interactions with Selenium." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/33173.

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Methylmercury (MeHg) is a ubiquitous contaminant and potent neurotoxicant with no completely effective therapy, although selenium antagonises MeHg toxicity. Furthermore, nanoparticles are promising as a novel drug delivery system. We researched the potential of selenium nanoparticles (SeNPs) in antagonising MeHg neurotoxicity compared to selenomethionine (SeMet) using primary astrocyte cell cultures and examining outcomes related to oxidative stress. We found that SeNPs were more toxic than SeMet. Increasing SeNPs significantly decreased MeHg cellular uptake and MeHg significantly decreased uptake of SeNPs at the highest concentration. Finally, SeNPs alone produced significantly higher reactive oxidative species and altered the ratio of reduced-to-oxidised glutathione, but MeHg, SeMet, and co-exposures did not. There were no significant effects on glutathione peroxidase or reductase activity. This suggests that SeNPs are more toxic than MeHg in cerebellar astrocytes and that they may not be suitable as a therapy at the doses and formulation used in this research.

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3

Heyes, Andrew. "Methylmercury in natural and disturbed wetlands." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=40361.

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Methylmercury (MeHg) is the most toxic species of mercury (Hg), and is an important ecosystem contaminant. In wetlands on the Canadian Shield, in NW Ontario, MeHg concentrations in peat and peat porewater ranged from 0.3 to 53 ng $ rm g sp{-1}$ and $<$0.1 to $ rm 7.3 ng l sp{-1},$ respectively. The greatest concentrations of MeHg occurred just below the water table, emphasizing the importance of redox reactions in Hg methylation. Methylmercury partition coefficients between peat and peat porewater ranged from $1.6 times 10 sp3$ to $8.6 times 10 sp5.$ No significant correlations between MeHg and concentrations of $ rm H sp+, NH sb4 sp+, NO sb3 sp-, NO sb2 sp-,$ total dissolved nitrogen (TDN), total dissolved phosphorus (TDP), $ rm SO sb4 sp{2-},$ and dissolved organic carbon (DOC) in the porewater of the wetlands were found.
Following shallow impoundment of a wetland, MeHg concentrations in the upper metre of peat porewater increased from $ rm 0.2 pm 0.2 ng l sp{-1}$ to $ rm 0.8 pm 0.8 ng l sp{-1}.$ Total mercury (T-Hg) and MeHg concentrations were determined in decomposing sedge, spruce needles, and Sphagnum moss, placed in a headwater wetland and the impounded wetland. The amount of T-Hg decreased in all tissues regardless of location. the amount of MeHg increased by as much as an order of magnitude in the tissues placed in the impounded wetland and wet areas (hollows and lawns) of the headwater wetland, but decreased in tissue placed in the dry areas (hummocks) of the headwater wetland. Therefore, it is during anaerobic decomposition of plant material that MeHg is produced in wetlands.
Incubations of peat were performed with addition of Hg, molybdate, $ rm SO sb4 sp{2-}, S sp{2-}, NH sb4NO sb3,$ pyruvate, and upland DOC. Methylmercury production was increased only after addition of $ rm SO sb4 sp{2-}$ and retarded only by $ rm NH sb4NO sb3.$ Although $ rm SO sb4 sp{2-}$ may not be required to methylate Hg, the increased availability of $ rm SO sb4 sp{2-}$ may influence the size and composition of the population of sulfate reducing bacteria in peat, thereby increasing the potential for Hg methylation.

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4

Hoffman, Nick(Nicholas D. ). "Modeling methylmercury in Maine's tribal meres." Thesis, Massachusetts Institute of Technology, 2018. https://hdl.handle.net/1721.1/122866.

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Thesis: S.B., Massachusetts Institute of Technology, Department of Earth, Atmospheric, and Planetary Sciences, 2018
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 59-76).
Methylmercury (MeHg) concentrations in the fish of twenty Maine lakes were projected for the year 2035 under three different policy scenarios. A mechanistic model of Hg fate and transport was calibrated for Maine's environment using four parameters: volumetric outflow rate, settling velocity, burial velocity, and Hg(II) biotic solids partitioning coefficient. The model was evaluated through comparison with measured results from the year 1993. The model results showed that the strictest global Hg regulations will lead to the greatest decreases in MeHg concentration. No piscivore will be safe for frequent consumption, even under the strictest regulations in the cleanest lakes. The Wabanaki traditional-subsistence diet will continue to entail unsafe MeHg exposures.
by Nick Hoffman.
S.B.
S.B. Massachusetts Institute of Technology, Department of Earth, Atmospheric, and Planetary Sciences

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5

Loseto, Lisa Lucia. "Methylmercury sources in the Canadian High Arctic." Thesis, University of Ottawa (Canada), 2003. http://hdl.handle.net/10393/26515.

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Mercury is increasing to toxic levels in Arctic biota living at the top of food webs. The rapid bioaccumulation and biomagnification of methylmercury (MeHg) in food chains, and the subsistence lifestyle of northern populations, has resulted in high levels of Hg in their blood. No prior measurements of MeHg sources to Arctic ecosystems have been made. In southern latitudes wetlands are considered important sources of MeHg with sulfate-reducing bacteria (SRB) thought to be responsible. Thus, the production of MeHg in Arctic wetlands was evaluated as well as SRB presence. Arctic wetlands were further evaluated as sources of MeHg in Arctic ecosystems, as well since snowmelt water provides 60 to 80% of water to Arctic terrestrial systems it was also evaluated as a source of MeHg. This was the first study to evaluate sources of MeHg entering Arctic ecosystems, and showed that although wetlands produced MeHg, the export to downstream lakes was dependant on site characteristics such as DOC levels, furthermore snowmelt water was the most significant source of MeHg to Arctic ecosystems measured here. (Abstract shortened by UMI.)

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6

Ruck, Philip Lawrence. "Cycling and Speciation of Mercury in Soils and Cadillac Brook and Hadlock Brook Watersheds, Acadia National Park, Maine." Fogler Library, University of Maine, 2002. http://www.library.umaine.edu/theses/pdf/RuckPL2002.pdf.

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7

Johnson, Kenneth B. "Fire and its Effects on Mercury and Methylmercury Dynamics for Two Watersheds in Acadia National Park, Maine." Fogler Library, University of Maine, 2002. http://www.library.umaine.edu/theses/pdf/JohnsonKB2002.pdf.

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8

Kaur, Parvinder. "Cellular and Molecular Mechanisms Behind Methylmercury-Induced Neurotoxicity." Doctoral thesis, Norwegian University of Science and Technology, Department of Neuroscience, 2008. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-2225.

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9

Bellum, Sairam. "Neurotoxic mechanisms of methylmercury: cellular and behavior changes." Texas A&M University, 2005. http://hdl.handle.net/1969.1/4992.

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The organic or methylated form of mercury (Hg), consisting of one methyl group bound to each atom of Hg, (methylmercury; MeHg), accounts for most of the Hg to which humans are exposed. MeHg, by virtue of its lipophilicity is highly neurotoxic to both the developing and mature central nervous system (CNS). Historically, MeHg has been implicated in high morbidity and mortality rates over the last 40 years in Japan, Iraq, Pakistan and Guatemala. The most common symptom exhibited in these exposure episodes was cerebellar ataxia. Recent in vitro studies using cultured granule cells showed that MeHg alters intracellular calcium ion ([Ca2+]i) homeostasis, potentiates reactive oxygen species (ROS) generation and loss of mitochondrial membrane potential leading to apoptotic death of cerebellar granule neurons. To better understand the neurotoxic mechanisms of MeHg on cerebellum, changes with respect to biochemical processes in cerebellar granule cells and associated behavior changes were investigated. The aims of this dissertation were: (1) to assess mercury concentrations in mouse brain using different routes of administration and different tissue preparations, (2) to determine the behavior effects of in vivo MeHg exposure in young adult mice. (3) to understand specific biochemical processes leading to granule cell death/dysfunction due to in vivo MeHg toxicity in mice, and (4) to determine the toxic effects of in vivo MeHg exposure on mice aged between 16-20 months. The present results showed that repeated oral exposure to MeHg results in greater accumulation of Hg in brain tissue when compared to single oral or subcutaneous exposures at the same concentration of MeHg. Behavior analysis revealed that MeHg at the concentrations used in this study had profound effects on motor coordination and balance in young adult and aged mice. Investigation of biochemical processes in cerebellar granule cells of mice exposed to MeHg showed an increase in ROS generation, alteration of ([Ca2+]i (in young adult mice) and loss of MMP in young adult and aged mice. However, these changes did not lead to apoptotic cell death of granule cells at the concentrations of MeHg used and at the specific time point it was investigated in young adult mice.

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10

Gibson, Jennifer C. W. "The effects of methylmercury ingestion on amphibian tadpoles." Thesis, University of Ottawa (Canada), 2006. http://hdl.handle.net/10393/27137.

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Methylmercury (MeHg) is a toxic heavy metal and a health threat to wildlife and humans, however nothing is known about its effects on amphibians. MeHg is produced from inorganic Hg in the aquatic environment, and bioaccumulates in the food chain. This exposes tadpoles to elevated levels of MeHg in their diet, and may pose a risk to development. Tadpoles of the North American species Bufo americanus and Rana pipiens as well as the African frog model species Xenopus tropicalis were subchronically exposed to dietary McHg ranging in concentration from 1ng/g to 1000 ng/g to determine LC50s and species sensitivity differences. A developmental differences study was also performed with B. americanus. The 33-day LC50 estimates indicate that Gosner stage 25 tadpoles of both B. americanus and R. pipiens were the most sensitive, and they exhibited a similar sensitivity to McHg toxicity. The X. tropicales LC50 estimate is significantly higher (p=0.05) than those calculated for B. americanus and R. pipiens Gosner stage 25, and the developmentally advanced B. americanus Gosner stage 27-30 LC50 estimate is also significantly higher (p=0.05) than the B. americanus Gosner stage 25 LC50. (Abstract shortened by UMI.)

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11

Drevnick, Paul Elliott. "METHYLMERCURY IN FISH: ACCUMULATION, TOXICITY, AND TEMPORAL TRENDS." Miami University / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=miami1180036291.

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12

Ogorek, Jacob. "Sediment methylmercury concentrations and production rates in coastal wetlands of Chequamegon Bay (WI), Lake Superior /." Connect to online version, 2009. http://minds.wisconsin.edu/handle/1793/45132.

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13

Sharin, Tasnia. "Methylmercury and Paraquat Induced Toxicity in the Mitochondria of Dopamine Neurons." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/35831.

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Methylmercury and Paraquat are environmental toxins that affect the central nervous system. Exposure to Paraquat and methylmercury causes movement impairments similar to the symptoms of Parkinson’s disease (PD). The degeneration of dopamine neurons due to mitochondrial dysfunction has been implicated in PD. This study investigates the mechanism of methylmercury and Paraquat induced mitochondrial dysfunction in dopamine neurons. Using in vitro assays, it was found that exposure to methylmercury (0.1-5µM) and Paraquat (300-500µM) inhibited complex I of the electron transport chain in mitochondria. This was associated with an increase in superoxide anion levels, decrease in superoxide dismutase activity, and loss of ATP. All of these factors led to the loss of mitochondrial membrane potential. Similar results were found in co-exposure treatment of 300µM of Paraquat with 0.1µM of methylmercury. These results indicate that methylmercury and Paraquat induce mitochondrial dysfunction causing the death of dopamine neurons.

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14

Wilcut, John Lance. "Methylmercury risk communication needs among women of childbearing age." Thesis, Montana State University, 2007. http://etd.lib.montana.edu/etd/2007/willcut/WillcutJ0507.pdf.

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While the consumption of fish is an essential part of the human diet, there are certain environmental toxins that reside within the earth's watersheds. One toxin in particular, methylmercury (MeHg) has been linked to neurotoxicity and consequent neuro-developmental health effects in growing fetuses and young children, even in minute doses. MeHg is known to accumulate in fish and fish products and with their consumption by women of childbearing age (WCBA), growing fetuses and young children are possibly placed in harm's way. To help prevent these health threats from occurring, guidelines and recommendations are placed into fish advisories by governmental agencies (federal, state, and tribal) through the application of the precautionary principle. The purpose of this study was to describe the risk communication status of the Montana fish consumption advisory in non-Native American women of childbearing age residing on an open reservation. Variables studied included fish consumption patterns, advisory awareness, risk awareness, and risk communication preferences. Secondary analysis of data compiled through a pilot study provided the cohort (n = 10) for this study. The majority regularly consumed fish (n = 7), while most denied prior knowledge of any fish advisory (n = 9). Half (n = 5) of the participants denied any knowledge about mercury contaminants in fish, while three stated they knew "only a little". This was emphasized through a series of true/false questions and with the majority (n = 9) having difficulty determining where the highest levels of mercury are found within a fish. A majority of the participants (n = 7) felt that they did not eat enough fish to worry about following the recommendations of the Montana Fish Consumption Guidelines. Important sources of health information to the cohort included: (a) doctors or other healthcare providers, (b) newsletters or brochures, (c) television, (d) magazines, (e) friends and relatives, and (f) government agencies. The results of this descriptive, hypothesis-generating study point to the need for larger scale studies involving non-Native rural women with the recommendations to include information on fish species, portions consumed, children of WCBA, userfriendly advisory pamphlets, and mercury exposure testing through hair and blood sampling.

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15

Hilmarsson, Torfi Geir. "Photodegradation of the neurotoxicant methylmercury (MeHg) in Swedish lakes." Thesis, Uppsala universitet, Institutionen för biologisk grundutbildning, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-275196.

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16

Li, Miling. "Environmental Origins of Methylmercury in Aquatic Biota and Humans." Thesis, Harvard University, 2016. http://nrs.harvard.edu/urn-3:HUL.InstRepos:27201754.

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Methylmercury (MeHg) is a neurotoxin found in fish and shellfish, that poses risks to human and ecological health. Exposure to MeHg adversely affects neurodevelopment of children and cardiovascular health in adults. Seafood consumption is the primary exposure route to MeHg in North America. An understanding of the link between environmental MeHg sources and human exposures is needed to determine the impacts of ongoing environmental change. However, few data exist for relating environmental exposures to human health outcomes. Imprecision in dietary recall data on fish consumption and variability in MeHg concentrations within and across seafood species consumed have made it challenging to accurately identify sources of human MeHg exposure. In addition, the diverse environmental sources of MeHg production in ecosystems make it more difficult to quantitatively attribute human exposures to specific environments where methylation is taking place. My doctoral dissertation uses naturally occurring mercury (Hg) stable isotopes to characterize sources of MeHg exposure in aquatic biota and human populations. The objectives of my work are to (1) explore the utility of Hg stable isotopes in human hair as a novel method for tracing sources of MeHg exposure to humans; (2) examine drivers of the internal body burden of MeHg in frequent seafood consumers; (3) refine understanding of environmental MeHg sources for estuarine fish. My first dissertation chapter characterizes the magnitude of mass-dependent fractionation between seafood and consumers and shows Hg stable isotopes in human hair is a promising tool for estimating different Hg exposure sources (e.g., coastal vs. oceanic fish). My second chapter uses dietary survey data and Hg isotopes in hair from high-frequency seafood consumers to show that differences in in vivo demethylation do not explain variability in biomarker concentrations. I infer that absorption efficiencies for MeHg in seafood are very low for some high-frequency fish consumers and hypothesize that this is caused by interactions with co-ingested foods. The last chapter investigates diverse Hg stable isotope signatures in benthic, riverine and pelagic estuarine fish and uses these signatures to better characterize the relative importance of different environmental MeHg sources.

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17

Thompson, Sally A. "Modulation of glutathione associated with methylmercury exposure in mice /." Thesis, Connect to this title online; UW restricted, 1996. http://hdl.handle.net/1773/8461.

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18

Merritt, Kristen K. "Assimilation of methylmercury by the green algae Selenastrum capricornutum." [Gainesville, Fla.] : University of Florida, 2002. http://purl.fcla.edu/fcla/etd/UFE1000144.

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Thesis (M.S.)--University of Florida, 2002.
Title from title page of source document. Document formatted into pages; contains ix, 43 p.; also contains graphics. Includes vita. Includes bibliographical references.

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19

Reed, Miranda Nicole. "Effects of dopamine challenges on clocked fixed-interval schedule performance for rats prenatally exposed to methylmercury and selenium." Auburn, Ala., 2007. http://repo.lib.auburn.edu/2007%20Spring%20Dissertations/REED_MIRANDA_25.pdf.

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20

Monrreal, Robert Horvath. "Hydrology and water chemistry in Weeks Bay, Alabama implications for mercury bioaccumulation /." Auburn, Ala., 2007. http://repo.lib.auburn.edu/2007%20Spring%20Theses/MONRREAL_ROBERT_35.pdf.

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21

Toms, Andrew David. "Mercury and methylmercury in the sediments of Lake St. Clair." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0018/MQ52669.pdf.

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22

Daré, Elisabetta. "Neurotoxicity of methylmercury : analysis of molecular mechanisms and behavioral alterations /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-145-4.

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23

Loupelle, Christianne. "Genotoxicity of methylmercury in North American river otters (Lutra canadensis)." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=80322.

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Methylmercury (MeHg) is the most toxic form of Hg to wildlife, partly because of its ability to biomagnify through the food chain. Previous studies have shown that river otter (Lutra canadensis) is particularly susceptible to increased exposure and body burdens of MeHg due to the piscivorous nature of its diet. The objectives of this study were to attempt to establish a relationship between MeHg concentrations in otter tissues and DNA fragmentation using single cell electrophoresis (comet assay) as well as evaluate the effectiveness of the comet assay as a tool in genotoxicity assessment in field samples. Results of preliminary experiments indicate that both time and storage temperature markedly influence the rate of spontaneous DNA degradation. Increased numbers of freeze/thaw cycling also appear to have a negative effect on DNA integrity. In addition, a cell culture experiment was set up to measure the effects of differing levels of MeHg on a neuroblastoma cell line.

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Walker, Rachel Alex. "Methylmercury Bioaccumulation in Spotted Salamanders (Ambystoma maculatum) in Southern Ohio." Wright State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=wright1496084470204606.

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25

Monteiro, Carlos Eduardo Salgueiro e. Silva. "Mercury and methylmercury in sediment cores from the Tagus estuary." Master's thesis, Universidade de Aveiro, 2010. http://hdl.handle.net/10773/4278.

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Mestrado em Ciências do Mar e das Zonas Costeiras
O mercúrio é actualmente considerado um dos metais mais nocivos para o ambiente. O presente trabalho incide sobre os factores que actuam sobre o mercúrio, influenciando a sua distribuição em ambientes estuarinos. Dado o histórico de contaminação no Estuário do Tejo, foram recolhidos cores de sedimentos e separadas as águas intersticiais em dois locais distintos: um fortemente contaminado, Cala do Norte, e outro não contaminado, Ponta da Erva. Os cores foram seccionados em camadas, tendo-se posteriormente analisado os teores de mercúrio total (HgT) e metilmercúrio (MeHg) na fracção sólida dos sedimentos e HgT e HgR, bem como MeHg dissolvidos nas águas intersticiais. As concentrações de HgT e MeHg foram relacionadas com outros parâmetros obtidos na fracção sólida e nas águas intersticiais, nomeadamente pH, Eh, O2 dissolvido, humidade, e as concentrações de LOI, Al, Si, Fe, Mn, Corg, DOC, Cl-, SO4 2- e HS-. Na Cala do Norte, a concentração de mercúrio total nos sedimentos variou entre 1 e 18 μg/g enquanto na Ponta da Erva foram determinados valores mais baixos, entre 0.4 e 0.5 μg/g. Em relação às concentrações de metilmercúrio, os valores variaram entre os não detectáveis (< 0.1 ng/g) e 87 ng/g na Cala do Norte e 0.54 ng/g na Ponta da Erva. Nos dois locais, apesar da diferença de concentrações, o HgT e MeHg mostraram-se encontrar-se em equilíbrio entre a fracção sólida e águas intersticiais. Os fluxos difusivos foram calculados na interface sedimento/água de modo a estimar a mobilidade das espécies de Hg e avaliar se existem trocas entre o sedimento e a coluna de água, considerando a toxicidade do MeHg. O fluxo estimado na Cala do Norte foi de 0.30 ng/m2d para o MeHg e 0.50 ng/m2d para HgR. Na Ponta da Erva, o fluxo de MeHg foi inferior ao calculado para a Cala do Norte, 0.19 ng/m2d, enquanto para o HgR foi maior, 1.13 ng/m2d. Estes fluxos evidenciam o transporte difusivo de Hg das águas intersticiais para a coluna de água em ambos os locais, reflectindo a importância das características do sedimento que potenciam os processos de metilação do Hg.
Mercury is currently considered one of the most harmful metals to the environment. This study focuses on factors that influence mercury distribution and its bioavailability in estuarine environments. Given the history of contamination in the Tagus estuary, sediment cores were collected and pore waters were separated from two sites: one heavily contaminated, Cala do Norte, and a non-contaminated, Ponta da Erva. In the laboratory, the levels of total mercury (Hg) and methylmercury (MeHg) in solid sediments and dissolved Hg (HgR and HgT) and MeHg in the pore waters were analyzed. Obtained Hg data were then compared to other parameters, namely the pH, Eh, dissolved O2, water content, as well the concentrations of LOI, Al, Si, Fe, Mn, Corg, DOC, Cl-, SO4 2- and HS-. In Cala do Norte, total mercury concentrations in sediments ranged between 1 and 18 μg/g while in Ponta da Erva, lower values were determined, ranging between 0.4 and 0.5 μg/g. Concentrations of methylmercury ranged between detection limit (< 0.1 ng/g) up to 87 ng/g in Cala do Norte and up to 0.54 ng/g in Ponta da Erva. In both places, despite the differences in concentrations, HgT and MeHg were in equilibrium between the pore waters and the solid fractions. The diffusive fluxes were calculated across the sediment/water interface in order to estimate the mobility of Hg species and assess whether there are exchanges between the sediment and water column, considering the MeHg toxicity. The estimated flux in Cala do Norte was 0.30 ng/m2d for MeHg and 0.50 ng/m2d for HgR. Conversely, in Ponta da Erva MeHg flux was lower than in Cala do Norte, 0.19 ng/m2d, while for HgR was higher, 1.13 ng/m2d. These fluxes evidence the diffusive transport of Hg from the pore waters to the overlying water in both sites reflecting the importance of sediment characteristics that enhance the Hg methylation processes.

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26

Hallberg, Åsa. "Thermodynamic stability of methylmercury complexes with low molecular mass thiols." Thesis, Umeå universitet, Kemiska institutionen, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-137289.

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27

Bodenrader, Jennifer. "Methylmercury Exposure via Canned Tuna Fish Consumption and Breast Cancer." ScholarWorks, 2016. https://scholarworks.waldenu.edu/dissertations/1992.

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Widespread consumption of canned tuna fish since the 1950s may explain some of the increase in breast cancer prevalence in the United States and Europe. Although canned tuna is the primary source of human exposure to methylmercury, its role as an estrogen activating metalloestrogen has been overlooked in the etiology and incidence of breast cancer. Carcinogenic theory asserts that increased exposure to estrogen elevates the risk of breast cancer. The purpose of this population-based, case control study was to examine the association between canned tuna consumption, total blood mercury, and breast cancer in the NHANES 2003-2006 surveys. A multivariable logistic regression model representing 138,747,398 U.S. adult females, controlling for covariates, was applied to investigate whether canned tuna consumption or blood mercury level had a relationship to breast cancer. According to study results, women who reported eating canned tuna at one level of increased frequency out of 11 had a 6.8% increased odds of being diagnosed with breast cancer (p =0. 000 OR 1.068 and 95% CI 1.067-1.069). Women with only a 0.01 Ug/L increase in total blood mercury level were found to have a 0.2% increased odds of being diagnosed with breast cancer (p =. 000 OR 1.002 and 95% CI 1.002-1.003). Additional research individuating the canned tuna fish variable in nutrition, fish, mercury, and breast cancer studies is recommended. This research contributes to positive social change by providing evidence to improve understanding and specification of canned tuna fish in future research and better identification of methylmercury levels in canned tuna fish for public knowledge.

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Nwobu, Ogochukwu L. "Methylmercury uptake and bioconcentration by the freshwater green alga Pseudokirchineriella subcapitata." Thesis, University of Ottawa (Canada), 2005. http://hdl.handle.net/10393/26997.

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Methylmercury (MeHg) enters most aquatic food webs primarily at the phytoplankton level. However, in the complex aquatic ecosystem, it is difficult to fully examine specific pathways. Consequently, in this study, the uptake of environmentally realistic levels of added MeHg concentrations (0.21 to 20 ng Hg L-1 ) by the freshwater green alga Pseudokirchniriella subcapitata grown in batch and semi-continuous cultures at biomass levels of (0.03, 0.15, 0.3 and 3 mg (dw) L-1) was investigated. In algal culture media without dissolved organic carbon (DOC) and in river water samples with DOC concentration of (2.8 mg L-1) uptake, uptake rate constant, algal concentration of MeHg and the bioconcentration factor (BCF) after 48 h was measured. MeHg uptake was biphasic, with rapid uptake of at least 50% of the total uptake taking place over the first 2 h of incubation followed by a more gradual uptake for the remaining 46 h. Desorption of MeHg from algal cells by re-suspension in acidic medium (pH 3) was < 10% of the total uptake at 48 h. Uptake rate constants of MeHg (ku) increased with aqueous MeHg concentration (r2 = 0.99). At 48 h, algal concentration of MeHg (MeHg (ng) divided by dry weight of algal biomass (g)) increased with aqueous MeHg concentration (r2 = 0.98) but decreased with increasing biomass (r2 = 0.75). This was shown to be a biomass dilution effect as the total uptake of MeHg did increase with biomass. Log MeHg BCF decreased with increasing algal biomass (r 2 = 0.99) with values of 6.9, 6.2 and 5.2 at 0.03, 0.3 and 3 mg (dw) L-1 respectively at all concentrations of MeHg added (0.5, 1.0 and 20 ng L-1).

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Sellers, Patricia. "Sediment flux and photodegradation of methylmercury in two boreal drainage lakes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq23661.pdf.

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30

Hunter, Allison M. "Methylmercury disassembles microtubules and induces apoptosis in P19 embryonal carcinoma cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ45228.pdf.

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31

Deikel, Stuart Mark. "Effects of methylmercury chloride on the social behavior of vervet monkeys." Thesis, McGill University, 1986. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=74016.

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Dulko-Smith, Beata. "Molecular dynamics studies of methylmercury interactions with the glucocorticoid receptor protein." Thesis, Umeå universitet, Kemiska institutionen, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-122070.

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Heath, John Charles Newland M. Christopher. "A behavioral procedure for measuring critical fusion frequency in rats." Auburn, Ala., 2005. http://repo.lib.auburn.edu/2005%20Summer/master's/HEATH_JOHN_9.pdf.

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Heath, John Charles Newland M. Christopher. "Neurobehavioral consequences of aging and chronic methylmercury exposure interactions with dietary selenium /." Auburn, Ala, 2008. http://repo.lib.auburn.edu/EtdRoot/2008/SUMMER/Psychology/Dissertation/Heath_John_22.pdf.

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35

Prodocimo, Maritana Mela. "Avaliação dos efeitos tóxicos do metilmercúrio na retina de duas espécies de teleósteos: Hoplias malabaricus e Danio rerio, utilizando um conjunto de biomarcadores biológicos." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/47/47135/tde-11122009-100626/.

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Em exposições especificamente relacionadas ao metilmercúrio (MeHg), o principal órgão alvo é o Sistema Nervoso Central (SNC). Os efeitos morfológicos do metilmercúrio nos fotorreceptores da retina de Hoplias malabaricus, traíra, foram investigados através de técnicas histopatológicas. Os exemplares de traíra foram distribuídos em três grupos: um grupo controle e dois grupos expostos ao MeHg. A contaminação trófica e subcrônica foi realizada através de exemplares vivos de Astyanax sp os quais receberam intraperitonealmente um volume de solução aquosa de MeHg correspondente a (0,075µg/g de traíra) ou (0,75µg/g de traíra). Quinze peixes por condição experimental foram sacrificados após 70 dias de exposição e os olhos foram coletados para as análises de microscopia de luz, microscopia eletrônica de transmissão e microscopia eletrônica de varredura. Através de análises químicas quantificamos o mercúrio em músculo e observamos em ambas as doses um acúmulo do metal. Para a maior dose do metal (0,75µg/g), as análises histopatológicas revelaram alterações nas membranas que unem os dois elementos de um cone pareado, degeneração da camada dos fotorreceptores e alterações morfológicas no segmento interno e segmento externo dos bastonetes. As análises também demonstraram alterações estruturais na membrana plasmática do segmento externo e alterações no processo de eliminação dos discos membranosos dos fotorreceptores. No momento da eliminação dos discos antigos foi observada a formação de vacúolos e também uma anormal eliminação dos discos membranosos pelas partes laterais do segmento externo. Para a menor dose do metal (0,075µg/g) além da alteração observada nas membranas que unem os cones pareados e da degeneração celular na camada dos fotorreceptores, observamos uma descontinuidade estrutural dos discos membranosos do segmento externo dos fotorreceptores. Todas estas alterações histopatológicas nos levam a concluir que o metilmercúrio induz alterações histopatológicas nas células da camada dos fotorreceptores podendo consequentemente trazer danos fisiológicos para toda a retina.
In exposures specifically related to methylmercury (MeHg), the main target organ is the Central Nervous System (CNS). In this study, morphological effects of methylmercury in retinal photoreceptors of Hoplias malabaricus, trahira, through histopathological techniques were investigated. Some mature fish were divided in three groups - one control group and the other two which were exposed to MeHg. The trophic and subchronic contamination was performed by live specimen of Astyanax sp which received a volume of aqueous solution of MeHg corresponding to (0,075µg /g trahira) or (0,75µg /g trahira). In an experimental condition, fifteen fish were sacrificed after 70 days of exposure and their eyes were collected for analysis of light microscopy, electron transmission microscopy and scanning electron microscopy. Through chemical analysis the amount of mercury found in muscle was quantified. In both doses an accumulation of the metal in the muscle of these animals was observed. For the highest dose of metal (0,75µg /g), the histopathological analysis revealed changes in the membrane that connects the two elements of a paired cone, cellular degeneration in the layer of photoreceptors and morphological changes in the internal and outer rod segments. The analysis also showed structural changes in the plasma membrane of the outer segment and changes in the process of removal of membranous discs in the apical region of a photoreceptor. At the time of disposal of old discs, the formation of vacuoles and also an abnormal membranous discs removal through the sides of the outer segment were observed. For the smallest dose of the metal (0,075µg/g) besides the morphological changes observed in the membrane which unites the paired cones and cellular degeneration throughout the layer of photoreceptors, a structural discontinuity of the membranous discs of the outer segment were observed in radial sections of rods. All these histopathological changes lead us to conclude that methylmercury induces morphological changes in cells of the layer of photoreceptors, and therefore causing physiological damage to the smooth functioning of the retina.

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Crump, Kate. "The effects of methylmercury on the reproductive axis of goldfish (Carassius auratus)." Thesis, University of Ottawa (Canada), 2008. http://hdl.handle.net/10393/27674.

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Methylmercury is both a potent neurotoxin and putative non-steroidal endocrine disruptor. Laboratory studies have provided evidence of reproductive impairment in many fish species after mercury exposure. Effects have been observed at every level of the reproductive axis including degeneration of neurons in the hypothalamus, decreased activity of gonadotrophs in the pituitary, and reduced steroidogenesis in the gonads. Despite the growing amount of research linking methylmercury exposure to reproductive impairment, the target tissues and mechanisms of action involved are still largely unknown. This thesis extends the body of evidence supporting the hypothesis that methylmercury is an endocrine disruptor in fish. To my knowledge, this is the first study to compare the effects of sub-chronic methylmercury exposure on adult goldfish at two different periods within the annual spawning cycle. The effects of endocrine disrupting toxins may differ depending on the season of exposure as goldfish exhibit seasonal fluctuations in gonad size, circulating sex steroids, and luteinizing hormone (LH). The present study demonstrates that ovarian steroidogenesis is impaired by methylmercury in both pre- and post-spawning fish. Analyses of pituitary and serum LH levels suggest that reductions in sex steroid levels are independent of alterations in LH. The possibility that reduced sex steroid levels in fish exposed to dietary methylmercury may be secondary to hypothalamic dysfunction remains to be addressed. Microarray analysis identified 59 genes differentially expressed in the hypothalamus after methylmercury accumulation. These candidate genes were categorized into discrete functional groups including apoptosis and stress response, calcium binding and transport, and protein synthesis, degradation, and transport. In addition, several neuroendocrine-related genes were differentially regulated including transcripts encoding peptides involved in stimulating the production and release of gonadotropin releasing hormone, secretion of LH, and gonadal steroidogenesis. This thesis demonstrates changes in the endocrine system linked to methylmercury exposure and provides the first step towards identifying the mechanistic relationship between changes in reproductive biomarkers and gene expression.

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Sundberg, Johanna. "Lactational transfer of methylmercury and inorganic mercury and uptake in the offspring /." Uppsala : Swedish Univ. of Agricultural Sciences (Sveriges lantbruksuniv.), 1999. http://epsilon.slu.se/avh/1999/91-576-5413-1.pdf.

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38

Harvey, Joel. "Environmental factors affecting Methylmercury in fish of the Laurentian Great Lakes region." Wright State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=wright1421076009.

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39

Engel, Gregory. "Effects of Methylmercury on Notch Targets and Motor Nerve Development in Drosophila." ScholarWorks @ UVM, 2013. http://scholarworks.uvm.edu/graddis/76.

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Methylmercury (MeHg) is a ubiquitous environmental toxin. Exposure to MeHg in humans occurs primarily through the consumption of contaminated seafood. MeHg has been shown to act most strongly during neural development. Epidemiological data on the effect MeHg exposure through seafood has on children and fetuses is conflicted, with large cohort studies showing both presence and absence of MeHg-induced deficits in achieving developmental milestones. Because of this uncertainty in the literature it is important that we come to understand the mechanisms of MeHg toxicity so that we might advise the public more accurately on the risks of MeHg exposure. Research into the mechanisms of MeHg toxicity has found a number of cellular and molecular effects including disruptions of microtubule formation, Ca2+ homeostasis, and glutamate signaling. However, none of these effects of MeHg fully explains its neurodevelopmental specificity. Previous work in Drosophila neural-derived cell lines has shown that MeHg causes upregulation of the canonical Notch response gene E(spl)m . The Notch pathway is crucial to neural development and perturbation of a Notch target may explain the developmental specificity of MeHg. In this dissertation I describe experiments I performed to test the hypothesis that the observed upregulation of E(spl)m plays an important role in MeHg toxicity in Drosophila. I first describe experimental evidence that E(spl)m is upregulated by MeHg treatment in vivo in Drosophila embryos in addition to cells, as has previously been shown. By contrasting the effects of the toxic inorganic mercurial HgCl2 with MeHg I show that the E(spl)m expression response to MeHg is not simply a stress response and is a likely specific activity of MeHg. I also show that the effect of MeHg on E(spl)m expression is not simply due to a developmental delay induced by the toxin. I also identify two neural phenotypes of MeHg toxicity in Drosophila embryos, in the outgrowth of the intersegmental and segmental motor nerves. Genetic manipulation causing overactivity of the Notch pathway in neurons can mimic these phenotypes. However, induced expression of E(spl)m in neurons does not cause a failure of motor nerve outgrowth. Upon further examination I demonstrate that endogenous expression of E(spl)m occurs in the muscle. Induced E(spl)m expression in the muscle causes a segmental nerve phenotype similar to MeHg treatment, indicating a role for E(spl)m in MeHg toxicity in this system. MeHg treatment and E(spl)m overexpression in the muscle causes a failure of normal muscle development. Yet, this gross developmental abnormality only partially explains the observed motor nerve phenotype. E(spl)m is unique among the E(spl) genes in its ability to cause these muscle and motor nerve phenotypes as shown by contrasting genetic manipulation of the closely related E(spl)m . Overall my findings support the hypothesis that MeHg toxicity in Drosophila is mediated in part by E(spl)m . They also suggest that E(spl)m plays an important role in the formation of the muscle during embryonic development, contributing to the literature describing disparate functions for E(spl) genes despite structural similarities. Finally, my findings suggest that MeHg may be able to impact neural development through toxicity in supporting tissues rather than neurons themselves. This final finding has implications for the study of MeHg toxicity in humans, and is supported by previous findings that describe a role of glia in modulating MeHg neurotoxicity.

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Lewis, Catherine Ann. "Sublethal Effects of Methylmercury on the Songbird Immune Response: An Experimental Study." W&M ScholarWorks, 2012. https://scholarworks.wm.edu/etd/1539626930.

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41

Malfa, Giuseppe Antonio. "Mechanism of action of Methylmercury on human astrocytes: neuroprotection of lipoic acid." Doctoral thesis, Università di Catania, 2014. http://hdl.handle.net/10761/1531.

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Astrocytes are actively involved in brain development, in mature CNS regulation and brain plasticity. They play a critical role in response to cerebral injuries and toxicants. A large amount of literature highlights the central role of astrocytes in mediating methylmercury (MeHg) neurotoxicity. In fact, mercury is the major neurotoxic pollutant that continues to arouse interest in research because of the severe risk it poses to human health. It has been widely demonstrated that this metal induces acute or chronic neurotoxicity exacerbating an oxidative stress condition and also age-related conditions, generating inflammatory reactions in the brain. These findings support the hypothesis that MeHg and many other environmental pollutants have the potential to cause neurodegeneration, through a variety of pathways similar to those described in human neurodegenerative diseases. However, despite numerous in vivo and in vitro studies, almost entirely on rat/mouse models, the issue remains controversial and the effects of MeHg in the human population are not completely known. Based on these findings, the aim of this study is to carry out for the first time, according to what has been reported in the literature, an in vitro experimental model that was as attributable as possible to humans, precisely human astrocytes (HA), so as to observe the effects of MeHg on some biochemical-molecular pathways. In parallel, I used HA cell cultures, which were treated with Alpha Dihydrolipoic Acid before being subjected to the action of MeHg in order to evaluate the possible protective effect exerted by this compound with antioxidant and chelating properties on cellular metabolism subjected to stress by MeHg.

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Wu, Pianpian. "Beneficial yet Risky : Evaluate Risks of Fish Diet of Mercury Exposure to Consumers in Sweden." Thesis, Uppsala universitet, Limnologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-179112.

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For a long time, fish is regarded as an important food source beneficial for human health. But there’s nowadays an increasing concern of fish consumption for increasing existence of mercury (Hg) and methylmercury (MeHg), which can be accumulated upon fish intake and pose health threats to human. It is suggested that children and pregnant women are more vulnerable to effects due to accumulation of Hg. There have been continuous efforts done by governments and researchers all over the world, e.g. publishing national and regional advisories on fish consumption, in order to inform public related risks aroused by excess fish consumption. Sweden, as one of the earliest countries abandons the use of Hg (Regeringskansliet, http://www.sweden.gov.se), has published a national advisory on fish consumption for pregnant and breastfeeding women (Swedish National Food Agency, SLV, http://www.slv.se/). Hg level in edible fish organs is also limited for safe consumption. In order to picture a better image of this, we investigated existed databases in Sweden on Hg levels in fish, fishery statistics, consumption data, and observed Hg level in human in recent decades for human exposure to Hg in Sweden. Though mercury emission decreased, the exposure to mercury via fish consumption is still high. We believe there’s a potential risk for Swedish inhabitants, especially pregnant women and women in breastfeeding, as well as young children. It is strongly recommended a safer limit of Hg in fish products for consumption in Sweden. We hope for more synthesized knowledge of safe fish consumption that benefit for the public and promote regional/national policy in having an up-to-date fish consumption advisory in Sweden.

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Baker, Julie Taylor Craig-Schmidt Margaret C. "Interactive effects of fish oil and methylmercury on the fatty acid profile of adult rat forebrain phospholipids." Auburn, Ala., 2007. http://repo.lib.auburn.edu/2007%20Fall%20Theses/Baker_Julie_23.pdf.

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Donlin, Wendy Dawn Newland M. Christopher. "The percentile IRT schedule high rate behavior as a tool for examining the toxic motor effects of methylmercury /." Auburn, Ala., 2005. http://repo.lib.auburn.edu/EtdRoot/2005/SPRING/Psychology/Dissertation/DONLIN_WENDY_59.pdf.

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45

Fallacara, Dawn. "Toxic effects of dietary methylmercury on immune system structure, function, and development in the American kestrel (Falco sparverius)." OpenSIUC, 2009. https://opensiuc.lib.siu.edu/dissertations/308.

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This dissertation summarizes three investigations in which immunosuppressive effects of environmentally relevant concentrations of dietary methylmercury (MeHg) were assessed in adult non-breeding male kestrels, female kestrels during egg laying, and nestling kestrels. Immunological endpoints included cell-mediated immunity (CMI) using the phytohemagglutinin (PHA) skin-swelling assay and antibody-mediated immune function using the sheep red blood cell (SRBC) hemagglutination assay. Hematology profiles were evaluated over time in adult males and nestlings to monitor immunological and physiological status of kestrels. Primary and secondary immune system organs were examined histopathologically to identify T and B cell-dependent structural changes related to immunosuppressive effects of MeHg. Male kestrels dosed with 3.9 µg/g MeHg in the diet for 13 weeks exhibited suppression of CMI (p = 0.019), elevation in the proportion of heterophils (p < 0.001) and total white blood cell counts (p < 0.001), and a decline in the proportion of peripheral blood lymphocytes (p < 0.001). Primary antibody-mediated immune response was suppressed at 0.6 µg/g MeHg (p = 0.014), but secondary immune function was not adversely effected. Female kestrels were dosed with 2.8 µg/g MeHg in the diet for 13 weeks prior to egg laying and exhibited a higher primary immune response to sheep red blood cells (SRBC) than controls (p = 0.013). Subtle reproductive effects were also apparent including a 4.3-day delay in egg laying (p < 0.001) and depletion of egg mass (p = 0.037), egg volume (p = 0.050), and eggshell thickness (p = 0.004). The quantity of antibody production during egg laying, as measured by anti-SRBC antibody concentrations in egg yolk, did not differ from controls. However, the duration of antibody production was significantly longer for MeHg dosed females (p = 0.007), suggesting immunomodulation occurred among dosed kestrels during egg laying. Nestlings dosed with 0.6 and 3.9 µg/g in the diet for 25 days post-hatch also exhibited suppression of CMI at 11 days of age (p = 0.004) and lymphoid depletion in spleen (p < 0.001) and thymus tissue (p = 0.017). Antibody-mediated immune function was not adversely affected in nestling kestrels. Results from these three investigations suggested suppression of CMI and lymphoid depletion occurred at a dose concentration of 3.9 µg/g MeHg in adult, non-breeding male kestrels and at both 0.6 and 3.9 µg/g MeHg dose concentrations in nestlings. Immunosuppressive effects and immune dysfunction with respect to antibody-mediated immune function occurred at a dose concentration of 2.8 µg/g in female kestrels during egg laying; estrogen-disrupting characteristics of MeHg during avian reproduction cannot be excluded as a potential influence on this response. Immunotoxic effects of dietary MeHg in female kestrels during egg laying were primarily immunosuppressive and targeted T cell-mediated immune function. Cell-mediated immunity was highly sensitive to the immunosuppressive effects of dietary MeHg at low, environmentally relevant exposure concentrations, and at comparatively high doses (> 3 ppm) at which reproductive effects have been demonstrated in kestrels in other investigations.

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46

Truong, Jocelyn. "The Cytotoxic Effects of Methylmercury on Cardiomyocytes: A Possible Implication for Heart Diseases?" Thesis, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/31687.

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Methylmercury (MeHg) is known predominantly as a neurotoxicant, however emerging experimental and epidemiological evidence has shown associations between MeHg exposure and the potential for increased risks of cardiovascular diseases. This thesis investigated the in vitro cytotoxic effects of MeHg in two cardiomyocyte cell lines, H9C2 rat neonatal cell line and AC16 adult human cell line. We observed significant increases in cell death at concentrations from 1 – 10 µM. ROS production and intracellular calcium concentrations increased dose-dependantly with MeHgCl exposure. Furthermore, while assessing mitochondrial function, a decline in maximal respiration at 1 µM was seen. However, these observations may in turn be a direct consequence of decreased cell numbers following exposures. Additionally, this study highlighted the differences in cellular bioenergetics which may impact how certain cells respond to contaminant stressors. The distribution of MeHg and total Hg in rat heart tissues was also examined and we observed increasing concentrations of MeHg in high and low dosed rat groups as compared to the vehicle controls. No difference was observed in Hg levels between the normal and high fat and sugar diet groups. The urinary isoprostane levels, which are indicative of systemic oxidative stress, showed significant increases in lean rats exposed to the high dose treatment. It was also observed that a high fat and sugar diet in lean and obese rats can contribute to increasing oxidative stress regardless of the level of contaminants they were dosed with. This thesis demonstrated several in vitro effects of MeHg on heart cells as well as determine the distribution of Hg levels in heart tissues and oxidative stress markers from an in vivo study.

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Davidson, Melissa Anne. "Fate and developmental effects of dietary uptake of methylmercury in Xenopus tropicalis tadpoles." Thesis, University of Ottawa (Canada), 2008. http://hdl.handle.net/10393/27676.

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To investigate the effects of methylmercury (MeHg) on development, Xenopus tropicalis tadpoles were exposed to MeHg diets with concentrations of 0.42 (control), 44 (low), and 270 (high) ng/g wet weight. Increased mortality, decreased metamorphosis, increased size, and a greater number of days between tadpoles reaching metamorphosis were observed in the high MeHg group, suggesting disruption to the thyroid axis. Triiodothyronine levels, however, were not significantly different between groups. In both the control and low MeHg groups, total Hg and MeHg body burdens increased rapidly, reached a plateau and eventually declined with a lower percent MeHg body burden. In the high MeHg group, body burden concentrations increased throughout the experiment. This study demonstrates that at low dosages of MeHg, elimination may prevent toxic exposure whereas at high dosages, demethylation and selective excretion mechanisms may be overwhelmed and disruption of development or death may occur in tadpoles.

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Bernhardsson, Malin. "Methylmercury in runoff from forested catchments : characterisation of three catchments prior to logging /." Uppsala : Sveriges lantbruksuniversitet, 2006. http://info1.ma.slu.se/IMA/Publikationer/internserie/2006-02.pdf.

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49

Lancaster, Nicole N. M. "Effects of salinity on biogeochemical processes and methylmercury production in freshwater wetland sediments." View electronic thesis, 2008. http://dl.uncw.edu/etd/2008-3//r1/lancastern/nicolelancaster.pdf.

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Spickler, Jessica Lynn. "Effects of Sub lethal Methylmercury Exposure on Pigment Coloration in a Model Songbird." W&M ScholarWorks, 2014. https://scholarworks.wm.edu/etd/1539626759.

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