Start Date

8-5-2020 12:00 AM

Document Type

Poster Session

Department

Biological Sciences

Advisor

Douglas Currie, PhD

Abstract

Recent research indicates that arsenic exposure through drinking water in Maine negatively affects IQ and learning in children (Wasserman et al., 2014). The mechanisms behind this neuropathy remain unknown and may be correlated with disruptions in glial cells. Arsenic exposure has been linked to increased reactive oxygen species (ROS) production, which damages the DNA, proteins, and lipids of cells (Barchowsky et al., 1999; Chen et al., 2009). ROS have also been implicated in the induction of neuronal autophagy (Scherz-Shouval & Elazar, 2007) where the cells metabolize cytosolic components during periods of oxidative stress. We hypothesized that arsenic exposure increases production of ROS in glial cells, thus inducing autophagy. To investigate the consequences of arsenic exposure on glia, we have measured the metabolic activity of a C6 glial cell line in the presence of varying arsenite concentrations. Our findings indicate that after a 48 hour period, cells exposed to 10 μM As(III) have an increased metabolism compared to cells incubated with the lower dose of 2.5 μM As(III). Cells exposed to 10 and 20 μM As(III) present with an abnormal rounded morphology and an absence of cell extensions. To determine if these findings are indicative of autophagy, lysosomal generation will be assessed. Cytoskeletal changes will be monitored in conjunction with previously conducted cytoskeletal stainings to analyze disruptions in microtubules and actin post-arsenic exposure.

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May 8th, 12:00 AM

Potential Induction of Autophagy Post-Arsenic Exposure in a C6 Glial Cell Line

Recent research indicates that arsenic exposure through drinking water in Maine negatively affects IQ and learning in children (Wasserman et al., 2014). The mechanisms behind this neuropathy remain unknown and may be correlated with disruptions in glial cells. Arsenic exposure has been linked to increased reactive oxygen species (ROS) production, which damages the DNA, proteins, and lipids of cells (Barchowsky et al., 1999; Chen et al., 2009). ROS have also been implicated in the induction of neuronal autophagy (Scherz-Shouval & Elazar, 2007) where the cells metabolize cytosolic components during periods of oxidative stress. We hypothesized that arsenic exposure increases production of ROS in glial cells, thus inducing autophagy. To investigate the consequences of arsenic exposure on glia, we have measured the metabolic activity of a C6 glial cell line in the presence of varying arsenite concentrations. Our findings indicate that after a 48 hour period, cells exposed to 10 μM As(III) have an increased metabolism compared to cells incubated with the lower dose of 2.5 μM As(III). Cells exposed to 10 and 20 μM As(III) present with an abnormal rounded morphology and an absence of cell extensions. To determine if these findings are indicative of autophagy, lysosomal generation will be assessed. Cytoskeletal changes will be monitored in conjunction with previously conducted cytoskeletal stainings to analyze disruptions in microtubules and actin post-arsenic exposure.

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