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.

No description available.

Methylmercury (MeHg) is a neurotoxic global pollutant that accumulates at high levels in predatory fish and marine mammals. The dietary intake of these animals is the main source of MeHg exposure in humans. At high levels, MeHg is known to damage the sensory and motor systems in both adults and children. Due to the complexity and inaccessibility of the central nervous system (CNS), early dysfunction is difficult to detect. Biochemical markers in the CNS have been used to identify MeHg neurotoxicity in animal models. Analogues of these biochemical targets are also present in peripheral blood tissue and may reflect early CNS dysfunction in human populations. The proposed peripheral biomarkers include (1) lymphocyte muscarinic acetylcholine (mACh) receptor, (2) serum cholinesterase (ChE) and (3) platelet monoamine oxidase (MAO). This thesis evaluates the effects of mercury (Hg) compounds on these CNS and peripheral biochemical markers in laboratory and epidemiological studies. In vitro studies showed that inorganic Hg (HgCl2) and MeHg inhibited mACh receptor binding in human, rat, and mouse brain tissue. Additionally, studies demonstrated that a low-level gestational exposure to MeHg reduced MAO activity in the developing embryo and in adult female offspring. Combined, these studies provide a framework for the assessment of biochemical targets of Hg compounds in humans. A cross sectional study was conducted to evaluate the association between peripheral biochemical markers and MeHg exposure in fish-eating adults (n=129) from Lac St-Pierre, Quebec. Blood-Hg concentrations were used as a marker of exposure and ranged from 0.2 to 17.0 mug/L. Multiple linear regression analysis demonstrated that both blood-Hg (p=0.011) and heavy smoking (p=0.001) were associated with reduced platelet-MAO activity. However, neither lymphocyte mACh receptor nor serum ChE was related to blood-Hg. These results suggest that exposure to MeHg may result in reduced plat

Filter-feeding macrozooplankton were collected from 24 lakes in south-central Ontario to examine relationships between environmental factors and methyl mercury accumulation. Zooplankton methyl mercury levels ranged from 19 to 448 ng$ rm cdot g sp{-1}$ dry weight in the study lakes and were highest in zooplankton from acidic brownwater lakes. Water color and lake water pH were the best predictors of methyl mercury levels in zooplankton explaining 73% of the variation. Methyl mercury concentrations were positively correlated with water color and inversely correlated with lake water pH. Water color explained a greater portion of the overall variance in methyl mercury levels, indicating that the supply of mercury from the drainage basin plays a key role in determining methyl mercury concentrations in the lacustrine biota. Zooplankton methyl mercury levels were well correlated with mercury concentrations in smallmouth bass (Micropterus dolomieui) and largemouth bass (Micropterus salmoides) from 11 of the study lakes showing zooplankton to be good indicators of the relative bioavailability of mercury at the base of the food chain.

Methylmercury (MeHg) is an environmental toxin to which we are exposed through the consumption of seafood. Reactive oxygen species (ROS) have been implicated in the mechanism of toxicity, and in vitro studies in our laboratory have implicated DNA oxidation, particularly the DNA repair enzyme oxoguanine glycosylase 1 (OGG1). My studies determined the effects of in utero exposure to MeHg on fetal brain DNA oxidation and postnatal neurodevelopmental deficits, and the role of ROS-mediated oxidative DNA damage using the free radical spin trap, α-phenyl-N-tert-butylnitrone (PBN), and DNA repair-deficient ogg1 knockout mice. While neither MeHg nor PBN altered DNA oxidation in fetal brain, MeHg caused cognitive deficits in passive avoidance and novel object recognition, the latter of which was blocked by PBN pretreatment, suggesting ROS involvement. Preliminary longevity studies following one litter from each treatment group to 16 months suggest that in utero MeHg treatment may shorten lifespan. Endogenous DNA oxidation was increased in the brains of ogg1 knockout fetuses compared to wild-type littermates, although this was not enhanced by MeHg. However, OGG1-deficient animals exhibited cognitive deficits in passive avoidance after MeHg treatment, suggesting a role for DNA damage. Furthermore, ogg1 knockout female mice exhibited a passive avoidance deficit compared to wild-type females regardless of treatment, corroborating a role for oxidative DNA damage in neurodevelopmental deficits. MeHg increased apoptosis in the hippocampal region of fetal brain, and may cause DNA double-strand breaks (DSBs), evidenced by enhanced phosphorylation of histone 2AX (γH2AX). Ogg1 knockout progeny exhibited increased cellular proliferation or migration in the developing hippocampal region, which was blocked by MeHg. My results provide the first evidence that: (1) MeHg may decrease lifespan; (2) PBN protects against some postnatal neurodevelopmental deficits caused by in utero exposure to MeHg; and (3) DNA repair-deficient progeny are more susceptible to postnatal cognitive deficits caused by in utero MeHg exposure, suggesting that ROS-mediated DNA oxidation plays a role in MeHg-initiated neurodevelopmental deficits.

Mercury concentrations in freshwater and marine biota are an ongoing concern, even in areas remote from local point sources, such as in the Canadian Arctic and sub-Arctic. Anadromous Arctic charr, which feed in the marine environment, have lower mercury concentrations than non-anadromous Arctic charr, which feed strictly in freshwater, but the two life-history forms have rarely been studied together, and the mechanisms driving the difference are unclear. Here, data from nine pairs of closely-located anadromous and non-anadromous Arctic charr populations were used to explore the impact of biological and life-history factors on individual total mercury concentration ([THg]) across a range of latitudes (49 – 81° N) in eastern Canada. From six of these sampling locations, additional samples of lower trophic level biota (i.e., algae, invertebrates, and forage fishes) were obtained in order to investigate patterns of total mercury (THg) and methylmercury (MeHg) biomagnification in the marine and lacustrine foodwebs supporting Arctic charr. Arctic charr mean [THg] ranged from 20 to 114 ng/g wet weight (ww) in anadromous populations, and was significantly higher in non-anadromous populations (all p < 0.01), ranging from 111 to 227 ng/g ww. Within-population variations in Arctic charr [THg] were best explained by fish age, and were also positively related to fork-length and δ15N-inferred trophic level. Across all sampling sites, the relationship between Arctic charr [THg] and fish age was significant and statistically similar in both life-history types, but only the non-anadromous fish demonstrated a significant relationship with trophic level. Fork-length and site latitude did not explain significant additional variation in Arctic charr [THg] across sampling locations. Trophic magnification factors were 1.98 – 5.19 for THg and 3.02 – 6.69 for MeHg in lacustrine foodwebs, and 1.59 – 2.82 for THg and 2.72 – 5.70 for MeHg in marine foodwebs, and did not differ significantly between the two feeding habitats for either THg or MeHg. The biomagnification rate of MeHg exceeded that of THg in both habitats. Mercury concentrations at the base of the foodweb were higher in the lacustrine environment (estimated at 17 – 139 ng/g dw for THg and 5 – 42 ng/g dw for MeHg) than in the marine environment (8 – 39 ng/g dw for THg and 1 – 11 ng/g dw for MeHg). The proportion of mercury in the methylated form was related to trophic level, and the relationship was statistically similar in the lacustrine and marine habitats. There was no effect of site latitude on mercury concentrations in marine or lacustrine biota, thus the difference between feeding habitats was consistent across a range of latitudes (56 – 72°N) in eastern Canada. We conclude that a difference in prey mercury concentration, driven by differential mercury concentrations at of the base of the lacustrine and marine foodwebs, is important for explaining the difference in mercury concentration between anadromous and non-anadromous in Arctic charr.

Methylmercury (MeHg) is a potent vertebrate neurotoxin and a contaminant of global concern. Increased anthropogenic emissions of mercury (Hg) to the atmosphere have led to increased bioaccumulation of MeHg in top predatory organisms such as fish, the consumption of which is the main exposure pathway of this toxin to humans and other animals. Forest canopies significantly increase the deposition of Hg in general to watersheds, but sources and fates of MeHg deposition in particular remain poorly understood. In this study, wet and dry loadings of MeHg to a watershed were quantified, and the retention and (photo)reduction of MeHg on foliage were measured using unique stable isotope experiments. We found that traditional methods of quantifying net deposition underestimate incoming sources of MeHg, and that retention of MeHg on forest canopies results in delayed transport of a significant portion of newly deposited MeHg from terrestrial catchments into adjacent lakes. / Ecology

Thesis (Ph. D.)--University of Nevada, Reno, 2008. / "May 2008." Includes bibliographical references. Online version available on the World Wide Web.

Thesis (Ph. D.)--University of Washington, 1996. / Vita. Includes bibliographical references (leaves [116]-124).

Thesis (M. Nursing)--Montana State University--Bozeman, 2007. / Typescript. Chairperson, Graduate Committee: Sandra Kuntz. Includes bibliographical references (leaves 63-67).