Submission Date

7-21-2017

Document Type

Paper- Restricted to Campus Access

Department

Biology

Faculty Mentor

Rebecca Kohn

Comments

Presented during the 19th Annual Summer Fellows Symposium, July 21, 2017 at Ursinus College.

Project Description

Reactive oxygen species (ROS) are known to cause neuronal damage, when they are not neutralized. Antioxidants, however, are able to combat the effects of ROS that may induce neurodegeneration. This study investigates the potential neuroprotective effects of the antioxidant cyanidin chloride, found in blueberries, on the nematode Caenorhabditis elegans (C. elegans), when subjected to oxidative stress via hydrogen peroxide. A wildtype and hyperactive strain of C. elegans are used in the study. The wildtype strain has a regularly functioning nervous system, while the hyperactive strain has a nervous system with increased release of neurotransmitters. This increased release is due to a mutation in the G protein gene, goa-1, of the C. elegans’ genome. In addition to treatment with an antioxidant, increased activity in the nervous system may provide additional aid in counteracting ROS. To measure the effects of cyanidin chloride post-exposure to hydrogen peroxide, fluorescent microscopy is used to observe and quantify the presence of neurons in both strains of C. elegans with and without the antioxidant. These dopaminergic neurons are labeled with Green Fluorescent Protein. This project provides a better understanding of the potential benefits of antioxidants on neurons the presence of ROS. Additionally, the results of the study may also show whether organisms with increased neurotransmitter release can better protect themselves against ROS in comparison to those with normally functioning nervous systems. Preliminary data suggest decreased neuronal loss in response to oxidative stress, following pre-treatment with cyanidin chloride.

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