Journal of Applied Physiology Journal of Applied Physiology
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J Appl Physiol 106: 311-315, 2009. First published November 20, 2008; doi:10.1152/japplphysiol.90737.2008
8750-7587/09 $8.00
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HIGHLIGHTED TOPIC
The Physiology and Pathophysiology of the Hyperbaric and Diving Environments

DNA damage after long-term repetitive hyperbaric oxygen exposure

Michael Gröger,1 Sükrü Öter,1,4 Vladislava Simkova,1,5 Markus Bolten,2 Andreas Koch,2 Volker Warninghoff,2 Michael Georgieff,1 Claus-Martin Muth,1 Günter Speit,3 and Peter Radermacher1

1Sektion Anästhesiologische Pathopyhsiologie und Verfahrensentwicklung and 3Abteilung Humangenetik, Universitätsklinikum, Ulm; 2Schifffahrtmedizinisches Institut der Marine, Kronshagen, Germany; 4Fizyoloji Anabilim Dali, Gülhane Askeri Tip Akademisi, Ankara, Turkey; and 5Anesteziologicko-resuscitacni klinika, Fakultni nemocnice u sv Anny, Brnó, Czech Republic

Submitted 9 June 2008 ; accepted in final form 12 November 2008

A single exposure to hyperbaric oxygen (HBO), i.e., pure oxygen breathing at supra-atmospheric pressures, causes oxidative DNA damage in humans in vivo as well as in isolated lymphocytes of human volunteers. These DNA lesions, however, are rapidly repaired, and an adaptive protection is triggered against further oxidative stress caused by HBO exposure. Therefore, we tested the hypothesis that long-term repetitive exposure to HBO would modify the degree of DNA damage. Combat swimmers and underwater demolition team divers were investigated because their diving practice comprises repetitive long-term exposure to HBO over years. Nondiving volunteers with and without endurance training served as controls. In addition to the measurement of DNA damage in peripheral blood (comet assay), blood antioxidant enzyme activities, and the ratio of oxidized and reduced glutathione content, we assessed the DNA damage and superoxide anion radical (O2bullet) production induced by a single ex vivo HBO exposure of isolated lymphocytes. All parameters of oxidative stress and antioxidative capacity in vivo were comparable in the four different groups. Exposure to HBO increased both the level of DNA damage and O2bullet production in lymphocytes, and this response was significantly more pronounced in the cells obtained from the combat swimmers than in all the other groups. However, in all groups, DNA damage was completely removed within 1 h. We conclude that, at least in healthy volunteers with endurance training, long-term repetitive exposure to HBO does not modify the basal blood antioxidant capacity or the basal level of DNA strand breaks. The increased ex vivo HBO-related DNA damage in isolated lymphocytes from these subjects, however, may reflect enhanced susceptibility to oxidative DNA damage.

combat swimmers; underwater demolition team divers; endurance training; comet assay; superoxide radical; superoxide dismutase; catalase; glutathione peroxidase



Address for reprint requests and other correspondence: P. Radermacher, Sektion Anästhesiologische Pathopyhsiologie und Verfahrensentwicklung Universitätsklinikum, Parkstrasse 11, D-89073 Ulm, Germany (e-mail: peter.radermacher{at}uni-ulm.de)







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