Approximately 10,000 tones of Hg are deposited annually as a result of anthropogenic activities. This increased Hg burden is known to have adverse neurological and reproductive effects on Common loons. A positive correlation between mercury (Hg) and selenium (Se) has been reported to exist in marine mammals and various species of marine and aquatic piscivorous birds. It has been hypothesized that the Hg/Se interactions may involve in the multiple mechanisms of Hg detoxification. This study focused on the suggested Hg/Se complex that forms in association with specific proteins. Specifically, this project focuses on the nature of these interactions in different tissues from wild Common loons (Gavia immer) that have been collected by the Canadian Wildlife Service. The Hg and Se concentrations in the various tissues were quantified using AAS. MALDI-TOF-MS and protein sequencing characterized the nature of the Hg/Se complex binding protein. Among the tissues, the liver had the highest concentrations of Hg and Se followed by kidney; muscle and brain. A strong association between Hg and Se was found in liver, kidney and eggs whereas there was no association in muscle and brain. In contrast brain and muscle had highest percentage of organic Hg suggesting that only inorganic Hg is associated with Se. Two Hg-Se binding protein complexes were found in liver both in the 15,200-15,300 Da range while one such complex in the same weight range was found in kidneys, when sequenced it was found that these proteins were the alpha A chain of Hemoglobin. The protein complex found in eggs was unique and although it was impossible to fully sequence it, it represents an unknown protein. The role of Se in Hg toxicity in eggs warrants further study.

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Mercury (Hg) is a toxicant of global concern, but few strategies exist to evaluate its biological effects on the ecosystem. Piscivorous wildlife, such as mink (Mustela vison), are particularly at risk because they can bioaccumulate Hg to concentrations known to impair neurological systems. Given that biochemical changes in the brain precede functional and structural impairments, I evaluated the use of neurochemicals as early-warning biomarkers of Hg toxicity in mink. Initial studies demonstrated that neurochemical biomarkers could be measured from mink carcasses collected from the field, as long as factors such as storage temperature and freeze thaw cycles were accounted for. To determine if Hg could directly impair neurochemicals in mink, an in vitro study demonstrated that Hg (HgCl2 and MeHg) could inhibit radioligand binding to the muscarinic cholinergic (mACh) receptor in the cerebellum and cerebral cortex regions of the brain. By analyzing whole brains collected from wild mink, it was demonstrated that a significant positive correlation existed between concentrations of brain Hg and levels of mACh receptors. These field observations were confirmed by results from a controlled methyl Hg (MeHg) feeding trial in captive mink, whereby sub-chronic exposure of mink to 0.5 - 2 ppm MeHg (ecologically relevant levels) resulted in significant increases in acetylcholinesterase activity and mACh receptor levels in specific brain regions. Collectively, these results demonstrated that exposure of mink to environmentally realistic concentrations of Hg can be related to alterations in neurochemicals at multiple tiers of biological organization. Given the importance of a functional nervous system in wildlife health, the physiological and ecological significance of these findings need further exploration. The results demonstrate that neurochemical approaches may be novel biomarkers to assess the ecotoxicology of Hg, and by extension, other pollutants o

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