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Mitochondrial respiration protects against oxygen-associated DNA damage

Author

Listed:
  • Ho Joong Sung

    (Translational Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health)

  • Wenzhe Ma

    (Translational Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health)

  • Ping-yuan Wang

    (Translational Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health)

  • James Hynes

    (Luxcel Biosciences Ltd, University College Cork)

  • Tomas C. O'Riordan

    (Luxcel Biosciences Ltd, University College Cork)

  • Christian A. Combs

    (Translational Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health)

  • J. Philip McCoy

    (Translational Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health)

  • Fred Bunz

    (Johns Hopkins University School of Medicine)

  • Ju-Gyeong Kang

    (Translational Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health)

  • Paul M. Hwang

    (Translational Medicine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health)

Abstract

Oxygen is not only required for oxidative phosphorylation but also serves as the essential substrate for the formation of reactive oxygen species (ROS), which is implicated in ageing and tumorigenesis. Although the mitochondrion is known for its bioenergetic function, the symbiotic theory originally proposed that it provided protection against the toxicity of increasing oxygen in the primordial atmosphere. Using human cells lacking Synthesis of Cytochrome c Oxidase 2 (SCO2−/−), we have tested the oxygen toxicity hypothesis. These cells are oxidative phosphorylation defective and glycolysis dependent; they exhibit increased viability under hypoxia and feature an inverted growth response to oxygen compared with wild-type cells. SCO2−/− cells have increased intracellular oxygen and nicotinamide adenine dinucleotide (NADH) levels, which result in increased ROS and oxidative DNA damage. Using this isogenic cell line, we have revealed the genotoxicity of ambient oxygen. Our study highlights the importance of mitochondrial respiration both for bioenergetic benefits and for maintaining genomic stability in an oxygen-rich environment.

Suggested Citation

  • Ho Joong Sung & Wenzhe Ma & Ping-yuan Wang & James Hynes & Tomas C. O'Riordan & Christian A. Combs & J. Philip McCoy & Fred Bunz & Ju-Gyeong Kang & Paul M. Hwang, 2010. "Mitochondrial respiration protects against oxygen-associated DNA damage," Nature Communications, Nature, vol. 1(1), pages 1-8, December.
    • Handle: RePEc:nat:natcom:v:1:y:2010:i:1:d:10.1038_ncomms1003
    DOI: 10.1038/ncomms1003
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    Cited by:

    1. Nathan P. Ward & Sang Jun Yoon & Tyce Flynn & Amanda M. Sherwood & Maddison A. Olley & Juliana Madej & Gina M. DeNicola, 2024. "Mitochondrial respiratory function is preserved under cysteine starvation via glutathione catabolism in NSCLC," Nature Communications, Nature, vol. 15(1), pages 1-17, December.

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