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.

Thesis--Wisconsin. / Vita. Includes bibliographical references (leaves 155-166).

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).

Thesis (M.S.)--University of Wisconsin -- La Crosse, 2009. / Includes bibliographical references (leaves 50-55)

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.

Thesis (M.S.) in Civil Engineering--University of Maine, 2002. / Includes vita. Includes bibliographical references (leaves 95-100).

Thesis (M.S.) in Ecology and Environmental Sciences--University of Maine, 2002. / Includes vita. Bibliography: leaves 55-61.

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.

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.

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.