Dopamine (DA) is a neurotransmitter that regulates movement, memory, pleasure, and motivation. Impaired dopamine production leads to Parkinson's Disease (PD), characterized by tremors, speech impediments, and memory loss. Levodopa (L-DOPA) is administered to increase dopamine levels in PD patients but can cause side effects like nausea, postural hypotension, and psychosis. Dopamine can autoxidize, generating free radicals responsible for cell death. We investigate whether L-DOPA mimics dopamine and how to protect cells. In the Hughes Lab, we use yeast (Saccharomyces cerevisiae) to study L-DOPA toxicity. Yeast have AA transporter, GAP1, that resembles the human L-amino acid transporter (LAT1). We engineered a yeast mutation that inhibits GAP1 internalization after AA homeostasis, allowing us to test the impact L-DOPA has on mitochondria and how it can lead to apoptosis. We conducted a dilution spot assay to identify the L-DOPA concentration that hinders cell growth followed by a 3.5-hour growth assay that determined cell mortality at specified concentration. Our next step involves introducing antioxidants and metals to L-DOPA-treated cells, aiming to rescue cell growth. L-DOPA is used to increase dopamine levels in PD but has drawbacks. We employ yeast as a model to assess L-DOPA toxicity, utilizing genetic modifications and assays to evaluate cell growth and mortality. Additionally, we explore the potential of antioxidants and metals to mitigate the harmful effects L-DOPA has on cells.