1 |
The effects of congenital methylmercury exposure on the developing hamster cerebellumReuhl, Kenneth Reynolds. January 1900 (has links)
Thesis (Ph. D.)--University of Wisconsin--Madison, 1980. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Bibliography; leaves 191-211.
|
2 |
Chronic methyl mercury toxicosis in guinea pigsJohnson, Allen Neill. January 1977 (has links)
Thesis--Wisconsin. / Vita. Includes bibliographical references (leaves 155-166).
|
3 |
Effect of methyl mercury on growth, reproduction and metabolism of guinea pigsHugunin, Alan Godfrey, January 1975 (has links)
Thesis (Ph. D.)--University of Wisconsin--Madison, 1975. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 220-229).
|
4 |
Sediment methylmercury concentrations and production rates in coastal wetlands of Chequamegon Bay (WI), Lake Superior /Ogorek, Jacob. January 2009 (has links)
Thesis (M.S.)--University of Wisconsin -- La Crosse, 2009. / Includes bibliographical references (leaves 50-55)
|
5 |
Methylmercury and Paraquat Induced Toxicity in the Mitochondria of Dopamine NeuronsSharin, Tasnia January 2017 (has links)
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.
|
6 |
Cycling and speciation of mercury in soils at Cadillac Brook and Hadlock Brook watersheds, Acadia National Park, Maine /Ruck, Philip Lawrence, January 2002 (has links)
Thesis (M.S.) in Civil Engineering--University of Maine, 2002. / Includes vita. Includes bibliographical references (leaves 95-100).
|
7 |
Fire and its effects on mercury and methylmercury dynamics for two watersheds in Acadia National Park, Maine /Johnson, Kenneth B., January 2002 (has links)
Thesis (M.S.) in Ecology and Environmental Sciences--University of Maine, 2002. / Includes vita. Bibliography: leaves 55-61.
|
8 |
Mass-independent Fractionation of Mercury Isotopes in Freshwater SystemsRose, Carla 13 January 2011 (has links)
Mass-independent fractionation (MIF) of Hg isotopes has the potential to track the environmental transport and fate of Hg. Herein we demonstrate that reducing both the frequency and intensity of light have a large effect on the expression and magnitude of MIF. This strongly supports the magnetic isotope effect as the mechanism behind MIF observed during aqueous photo-reduction of Hg(II) and MeHg. The ratios of MIF, KapDelta199Hg/KapDelta201Hg, were 1.00 ± 0.04 (2SE) for Hg(II) and 1.35 ± 0.16 (2SE) for MeHg respectively and did not change as incident radiation energy and magnitude of MIF diminished, suggesting the respective MIF pathways remained constant regardless of experimental conditions. Comparable amounts of total photo-reduction were shown to coincide with different magnitudes of MIF depending the wavelength light available for photo-reduction. This confirms there are multiple pathways for photo-reduction in freshwater reservoirs and indicates that quantitatively relating photo-reduction and MIF will be challenging.
|
9 |
Mass-independent Fractionation of Mercury Isotopes in Freshwater SystemsRose, Carla 13 January 2011 (has links)
Mass-independent fractionation (MIF) of Hg isotopes has the potential to track the environmental transport and fate of Hg. Herein we demonstrate that reducing both the frequency and intensity of light have a large effect on the expression and magnitude of MIF. This strongly supports the magnetic isotope effect as the mechanism behind MIF observed during aqueous photo-reduction of Hg(II) and MeHg. The ratios of MIF, KapDelta199Hg/KapDelta201Hg, were 1.00 ± 0.04 (2SE) for Hg(II) and 1.35 ± 0.16 (2SE) for MeHg respectively and did not change as incident radiation energy and magnitude of MIF diminished, suggesting the respective MIF pathways remained constant regardless of experimental conditions. Comparable amounts of total photo-reduction were shown to coincide with different magnitudes of MIF depending the wavelength light available for photo-reduction. This confirms there are multiple pathways for photo-reduction in freshwater reservoirs and indicates that quantitatively relating photo-reduction and MIF will be challenging.
|
10 |
Neurotoxic mechanisms of methylmercury: cellular and behavior changesBellum, Sairam 25 April 2007 (has links)
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.
|
Page generated in 0.0539 seconds