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Menadione Induces DNA Damage and Superoxide Radical Level In HEK293 Cells

Received: 15 November 2019     Accepted: 2 December 2019     Published: 11 December 2019
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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.

Published in Cell Biology (Volume 7, Issue 2)
DOI 10.11648/j.cb.20190702.11
Page(s) 14-22
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2019. Published by Science Publishing Group

Keywords

Reactive Oxygen Species (ROS), Menadione, Oxidative Stress, Superoxide Radical, Neurodegenerative Diseases

References
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Cite This Article
  • APA Style

    Alireza Ghodsi Senejani, Joseph Matthew Magrino, Amanda Marston, Michelle Gregoire, Khoa Dang Dinh. (2019). Menadione Induces DNA Damage and Superoxide Radical Level In HEK293 Cells. Cell Biology, 7(2), 14-22. https://doi.org/10.11648/j.cb.20190702.11

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    ACS Style

    Alireza Ghodsi Senejani; Joseph Matthew Magrino; Amanda Marston; Michelle Gregoire; Khoa Dang Dinh. Menadione Induces DNA Damage and Superoxide Radical Level In HEK293 Cells. Cell Biol. 2019, 7(2), 14-22. doi: 10.11648/j.cb.20190702.11

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    AMA Style

    Alireza Ghodsi Senejani, Joseph Matthew Magrino, Amanda Marston, Michelle Gregoire, Khoa Dang Dinh. Menadione Induces DNA Damage and Superoxide Radical Level In HEK293 Cells. Cell Biol. 2019;7(2):14-22. doi: 10.11648/j.cb.20190702.11

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  • @article{10.11648/j.cb.20190702.11,
      author = {Alireza Ghodsi Senejani and Joseph Matthew Magrino and Amanda Marston and Michelle Gregoire and Khoa Dang Dinh},
      title = {Menadione Induces DNA Damage and Superoxide Radical Level In HEK293 Cells},
      journal = {Cell Biology},
      volume = {7},
      number = {2},
      pages = {14-22},
      doi = {10.11648/j.cb.20190702.11},
      url = {https://doi.org/10.11648/j.cb.20190702.11},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.cb.20190702.11},
      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.},
     year = {2019}
    }
    

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  • TY  - JOUR
    T1  - Menadione Induces DNA Damage and Superoxide Radical Level In HEK293 Cells
    AU  - Alireza Ghodsi Senejani
    AU  - Joseph Matthew Magrino
    AU  - Amanda Marston
    AU  - Michelle Gregoire
    AU  - Khoa Dang Dinh
    Y1  - 2019/12/11
    PY  - 2019
    N1  - https://doi.org/10.11648/j.cb.20190702.11
    DO  - 10.11648/j.cb.20190702.11
    T2  - Cell Biology
    JF  - Cell Biology
    JO  - Cell Biology
    SP  - 14
    EP  - 22
    PB  - Science Publishing Group
    SN  - 2330-0183
    UR  - https://doi.org/10.11648/j.cb.20190702.11
    AB  - 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.
    VL  - 7
    IS  - 2
    ER  - 

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Author Information
  • Department of Biology and Environmental Science, University of New Haven, West Haven, USA

  • Department of Biology and Environmental Science, University of New Haven, West Haven, USA

  • Department of Biology and Environmental Science, University of New Haven, West Haven, USA

  • Department of Biology and Environmental Science, University of New Haven, West Haven, USA

  • Department of Mathematics, University of New Haven, West Haven, USA

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