Date Thesis Awarded
Bachelors of Science (BS)
Methylmercury is a widespread, highly neurotoxic, pollutant that is well known to cause neurological deficits and is particularly harmful during neural development. Many studies have investigated the neurotoxic effects of MeHg to better comprehend the threat that MeHg exposure poses to organisms. However, few studies have focused on the molecular and cellular effects that MeHg has on developing avian species, let alone altricial songbirds. Even less is understood how maternal MeHg deposits affect and disrupt the developing nervous system of songbird species. To address this issue, the objective of this study was to investigate the effects of maternally deposited MeHg on neural proliferation and apoptosis of the developing zebra finch (Taeniopygia guttata) embryo. The study also investigated the toxicokinetics of MeHg during embryonic zebra finch development, to provide insight into which stages of development may be more susceptible to the harmful effects of MeHg due to increased exposure. We used in situ hybridization (ISH) for proliferating cell nuclear antigen (PCNA), Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) along with cell counting techniques to respectively determine any changes in proliferation and apoptosis in the developing neural regions of stage 25 embryos in control and 2.4ppm developmentally exposed embryos. We found a statistically significant decrease in neural proliferation in the midbrain of 2.4ppm embryos, but no significant difference was found in the amounts of apoptosis between control and MeHg exposed embryos. The mercury content was measured in a developing egg’s pooled yolk and albumin, and embryo order to elucidate MeHg toxicokinetics at stage 25, stage 32, and stage 38 embryos. We found a trend of increased mercury accumulation in the embryo as development progressed.
Stančiauskaitė, Monika E., "The Effects of Methylmercury on Cell Proliferation and Apoptosis during Zebra Finch Neural Development" (2015). Undergraduate Honors Theses. Paper 211.