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    Reactive oxygen species, mitochondria, and endothelial cell death during in vitro simulated dives

    Access Status
    Fulltext not available
    Authors
    Wang, Q.
    Guerrero, F.
    Mazur, A.
    Lambrechts, K.
    Buzzacott, Peter
    Belhomme, M.
    Theron, M.
    Date
    2015
    Type
    Journal Article
    
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    Citation
    Wang, Q. and Guerrero, F. and Mazur, A. and Lambrechts, K. and Buzzacott, P. and Belhomme, M. and Theron, M. 2015. Reactive oxygen species, mitochondria, and endothelial cell death during in vitro simulated dives. Medicine and Science in Sports and Exercise. 47 (7): pp. 1362-1371.
    Source Title
    Medicine and Science in Sports and Exercise
    DOI
    10.1249/MSS.0000000000000563
    ISSN
    0195-9131
    School
    School of Nursing, Midwifery and Paramedicine
    URI
    http://hdl.handle.net/20.500.11937/73288
    Collection
    • Curtin Research Publications
    Abstract

    © 2014 by the American College of Sports Medicine. Purpose Excessive reactive oxygen species (ROS) is considered a consequence of hyperoxia and a major contributor to diving-derived vascular endothelial damage and decompression sickness. The aims of this work were: 1) to directly observe endothelial ROS production during simulated air dives as well as its relation with both mitochondrial activity and cell survival; and 2) to determine which ambient factor during air diving (hydrostatic pressure or oxygen and/or nitrogen partial pressure) is responsible for the observed modifications. Methods In vitro diving simulation was performed with bovine arterial endothelial cells under real-time observation. The effects of air diving, hydrostatic, oxygen and nitrogen pressures, and N-acetylcysteine (NAC) treatment on mitochondrial ROS generation, mitochondrial membrane potential and cellular survival during simulation were investigated. Results Vascular endothelial cells performing air diving simulation suffered excessive mitochondrial ROS, mitochondrial depolarization, and cell death. These effects were prevented by NAC: after NAC treatment, the cells presented no difference in damage from nondiving cells. Oxygen diving showed a higher effect on ROS generation but lower impacts on mitochondrial depolarization and cell death than hydrostatic or nitrogen diving. Nitrogen diving had no effect on the inductions of ROS, mito-depolarization, or cell death. Conclusion This study is the first direct observation of mitochondrial ROS production, mitochondrial membrane potential and cell survival during diving. Simulated air SCUBA diving induces excessive ROS production, which leads to mitochondrial depolarization and endothelial cell death. Oxygen partial pressure plays a crucial role in the production of ROS. Deleterious effects of hyperoxia-induced ROS are potentiated by hydrostatic pressure. These findings hold new implications for the pathogenesis of diving-derived endothelial dysfunction.

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