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Oxidative stress in cells is caused by reactive oxygen species (ROS) if there is a deficiency of necessary antioxidants to neutralize them. ROS, which work through free radicals, oxidize sites on endogenous neurotransmitters and other important cellular components that allow cells to function properly including dopamine. When cellular components are oxidized, they are unable to continue normal functioning and will eventually die through apoptosis. This cell death can contribute to the neurodegeneration seen in Parkinson’s disease. Increased intracellular dopamine allows more oxidation sites for ROS within the cell contributing to further neurodegeneration. It is believed that lower levels of dopamine within the cell can lead to a prolonged or inhibition of neurodegeneration which can be simulated using a mutation in the dopamine reuptake transporter. Within the model organism Caenorhabditis elegans crossed with GFP, one can visually determine the effects of low intracellular dopamine on neurodegeneration using a mutation in the dopamine transporter, dat-1. Hydrogen peroxide survival assays were executed showing a statistically significant increase in the death of homozygous GFP worms when compared to the developed cross strain containing homozygous GFP and dat-1 mutations, suggesting that the dat-1 mutation protects the worm from death via oxidative stress. Statistical analysis was done using the Student T-Test with the Bonferroni Adjustment. Preliminary data for the fluorescent microscopy is currently inconclusive. Future research will continue fluorescent microscopy to visualize and quantify dopaminergic neuron degeneration. All data was generated in Dr. Rebecca Kohn’s Lab at Ursinus College.
Carter, Bryan P., "Effects of Reduced Intracellular Dopamine on Apoptosis in the Dopaminergic Neurons of Caenorhabditis elegans" (2016). Biology Honors Papers. 8.