Superoxide induced oxidative stress mediate DNA damage and neuronal death Alireza Senejani1, Joseph M. Magrino1, Amanda Marston1 1Department of Biology and Environmental Science, University of New Haven, West Haven, CT 06516
Reactive oxygen species (ROS) can damage cellular components, including mitochondrial and genomic DNA. Oxidized DNA can transgress into lethal double stranded breaks if not adequately repaired. Clinical reports of the major neurodegenerative diseases have denoted the presence of oxidized genomic DNA with no clear understanding of their role in disease progression. To date, little is known on the neuronal vulnerability and repair kinetics of oxidative damage. We induce oxidative stress to study how neuronal repair kinetics contributes to reduce neuronal viability in oxidative stress conditions. Results of our study suggest that neuron cells have a significantly reduced viability in response to Menadione compared to fibroblasts. Higher levels of superoxide anions are believed to induce extensive genomic DNA damage. COMET analysis suggested that cells had regressed DNA repair kinetics in response to oxidative stress and increased level of DNA breaks could be the cause behind the reduced viability. Pretreatment of cells with antioxidant can reduces ROS and decreases DNA damage indicating the oxidative stress was the cause of induced level of cell death. Results of our finding indicate oxidative stress effects neurodegeneration and potential use and impact of antioxidant therapeutic agents for neurodegenerative disorders.
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