Effects of Nicotine and Indole-3-carbinol on Rotenone-induced Drosophila model of Parkinsons disease. Cassie K. Huang, Jessie Rottersman, S. Tariq Ahmad. Biology, Colby College, Waterville, ME.

   Parkinson's disease (PD) is a neurodegenerative disorder primarily affecting the dopaminergic neurons in the nigrostriatal pathway resulting in debilitating motor impairment in both familial and sporadic cases. Chronic exposure to the pesticide rotenone also selectively degenerates dopaminergic neurons and causes locomotor impairment and early mortality in a Drosophila model of chemically-induced PD. Nicotine, a nicotinic acetylcholine receptor agonist, produces stimulant effects on animals. It is widely consumed by humans, and substantial losses in nicotinergic receptors have been found postmortem in Parkinsons disease. Previous research has shown positive results using nicotine to treat rotenone toxicity in vitro. Indole-3-carbinol (I3C) is found naturally in many cruciferous vegetables such as brussel sprouts, kale, and broccoli. It is thought to have antioxidant effects and has been targeted as a possible cancer treatment after a study showed I3C dose-related decreases in tumor susceptibility. This study investigated the effects of nicotine and indole-3-carbinol on early mortality in a rotenone-induced PD model. We show that treatment with 10 uM nicotine and 1mM indole-3 carbinol-supplemented food improve the early mortality in flies. The recovery of rotenone-induced locomotor deficits by nicotine and indole-3-carbinol is currently being explored. Furthermore, future studies will explore the antioxidant effects of these two drugs through a superoxide dismutase (SOD) assay.