Investigation of the Protective Role of H­2s in a Cell Culture Model of Parkinson’s Disease

Parkinson’s disease (PD) is the second most common neurodegenerative disease, characterized by the loss of dopaminergic (DA) neurons in the substantia nigra of midbrain. Although the cause for selective death of DA neurons is not completely understood, mitochondrial dysfunction followed by reactive oxygen species (ROS) accumulation is thought to be a contributory factor. Reduction of oxidative stress is considered to be a potential strategy to halt or slow down the disease progress. The gasotransmitter molecule hydrogen sulfide (H₂S) is known to have antioxidant properties within cells and provides cytoprotection via multiple additional mechanisms. In this work, we investigate a novel, slow H₂S-releasing molecule N-thiocarboxyanhydride-1 (NTA1), as a potential candidate to rescue neuronal injury from ROS accumulation. Mitochondrial damage and ROS accumulation was induced in SH-SY5Y cells by exposure to rotenone. Using this in vitro model of PD, any beneficial effects of NTA1 treatment is currently being tested. Preliminary results suggest a protective role of NTA1 pre-treatment on rotenone-induced apoptosis.