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/Advisor

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