Yellow Dye No. 5, also known as tartrazine (TRZ), is widely used[1] and has an accepted daily intake (ADI) of 0-7.5 mg/kg of body weight per day[2]. Consuming TRZ dosages greater than the ADI can lead to reduced levels of antioxidant enzymes in the brain, chromosomal alterations, or neuronal dendritic changes, [3, 4] which can result in oxidative stress, impaired neuronal functioning and potential mutagenic effects. Within the ADI, there have been observed reductions of the copper zinc superoxide dismutase-1 (SOD1) enzyme levels.[5]We hypothesize that TRZ interacts pre-translationally inside the cell, resulting in the reduction of SOD1 mRNA. In this study, differentiated Neuro2A-derived neurons were exposed to TRZ for 3 or 7 days. We tested a concentration curve from 0 to 11 μg/mL. Treated cells were grown on poly-L-lysine (PLL)- and laminin-coated glass coverslips, immunostained with anti-β-tubulin III and phalloidin, imaged, and analyzed using NeuronJ/ImageJ (NIH). Neurons were traced to analyze the morphological impacts of TRZ. SOD1 mRNA was quantified using reverse transcription quantitative polymerase chain reaction (RT-qPCR). We analyzed the differences in SOD1 mRNA levels of the controls vs. experimental cells, using the 2-ΔΔCT statistical method. We found that TRZ caused an increase in neurite length and a general decreasing trend of SOD1 mRNA expression. The reduction in SOD1 mRNA expression could indicate possible pre-translational modifications, which could be a result of TRZ’s ability to bind DNA. These findings help fill the gap in understanding the mechanism of SOD1 downregulation due to TRZ exposure.

Thesis Completion




Thesis Chair

Hawthorne, Alicia


Bachelor of Science (B.S.)


College of Medicine


Burnett School of Biomedical Sciences

Degree Program

Biomedical Sciences



Access Status

Open Access

Release Date


Restricted to the UCF community until 5-1-2022; it will then be open access.