Menadione Induces DNA Damage and Superoxide Radical Level In HEK293 Cells
Alireza Ghodsi Senejani,
Joseph Matthew Magrino,
Amanda Marston,
Michelle Gregoire,
Khoa Dang Dinh
Issue:
Volume 7, Issue 2, December 2019
Pages:
14-22
Received:
15 November 2019
Accepted:
2 December 2019
Published:
11 December 2019
Abstract: 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. Here, we studied how DNA repair kinetics contributes to reduce neuronal viability in oxidative stress conditions. To induce internal oxidative stress, we exposed neuronal-like HEK293 and fibroblast cells to 2-Methyl-1, 4-napthoquinone (Menadione). We found HEK293 cells have a reduced viability in response to induced oxidative stress compared to fibroblasts. Furthermore data obtained from COMET analysis show increased level of DNA breaks and regressed DNA repair kinetics in treated cells. Our results show that HEK293 cells have a regressed repair kinetics that allows for oxidative damage to transgress into lethal forms of DNA damage. Our findings indicate that oxidative stress can play a key role in neurodegenerative diseases and alleviation of their presence could increase neuronal survival.
Abstract: 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 dise...
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