Date Awarded


Document Type


Degree Name

Master of Science (M.Sc.)




Daniel Cristol

Committee Member

Eric Bradley

Committee Member

John Swaddle

Committee Member

Paul Heideman


Anthropogenic activities such as burning of fossil fuels, mining, and industrial processes continue to increase the levels of mercury circulating in the environment. Once methylated, mercury can be incorporated into animal tissues, causing it to biomagnify up the food web. Deleterious fitness impacts are commonly associated with increased mercury content in birds. The mechanistic pathway to those effects on fitness needs further research in order to develop appropriate remediation efforts and predict future harm on bird populations. Oxidative stress is proposed as one of the primary ways though which mercury causes accumulation of cellular damage. Well-documented cases of mercury induced oxidative stress indicate an increased level of reactive oxygen species along with a depletion of protective antioxidant molecules. We assessed the relationship between dietary mercury exposure and activity levels of superoxide dismutase (SOD) isozymes to evaluate the ability of SOD to serve as a non-lethal biomarker of oxidative stress. We approached this goal in two ways. First, we monitored levels of extracellular SOD in the blood throughout the lifetime of zebra finches exposed to mercury only during development. We found no effect of developmental mercury exposure on SOD3 activity levels, but found significant effects of age and sex. Second, we examined the effect of lifetime mercury exposure and acute exercise on adult zebra finches. Again, mercury did not induce significant changes in SOD3 activity levels, however, sex did play a role in dictating SOD3 activity levels in the blood. We detected a small non-significant effect of mercury on liver, similar to that reported in Henry et al. (2014). This suggests that blood SOD3 activity levels may not be a viable option for quantifying mercury-induced oxidative stress, mammalian models suggest that this is because mercury interacts with each SOD isozyme differently. Mitochondrial SOD seems to be more susceptible to decreased activity levels from mercury than extracellular SOD. We found that sex is playing a crucial role in dictating SOD3 activity levels, likely due to estrogen’s role as an antioxidant, as previously demonstrated in mammalian models. This is the first in-depth analysis of the mercury, sex, exercise, and age activity levels as predictors of SOD3 in the plasma of songbirds. Because SOD3 activity sampled simultaneously in the liver and plasma of individuals did not correlate, SOD3 is not useful as a biomarker for Oxidative stress in zebra finches.



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