Weber, Stefan U; Koch, Andreas; Kankeleit, Jens; Schewe, Jens-Christian; Siekmann, Ullrich; Stüber, Frank; Hoeft, Andreas; Schröder, Stefan (2009). Hyperbaric oxygen induces apoptosis via a mitochondrial mechanism. Apoptosis, 14(1), pp. 97-107. New York, N.Y.: Springer 10.1007/s10495-008-0280-z
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During therapeutic hyperbaric oxygenation lymphocytes are exposed to high partial pressures of oxygen. This study aimed to analyze the mechanism of apoptosis induction by hyperbaric oxygen. For intervals of 0.5-4 h Jurkat-T-cells were exposed to ambient air or oxygen atmospheres at 1-3 absolute atmospheres. Apoptosis was analyzed by phosphatidylserine externalization, caspase-3 activation and DNA-fragmentation using flow cytometry. Apoptosis was already induced after 30 min of hyperbaric oxygenation (HBO, P < 0.05). The death receptor Fas was downregulated. Inhibition of caspase-9 but not caspase-8 blocked apoptosis induction by HBO. Hyperbaric oxygen caused a loss of mitochondrial membrane potential and caspase-9 induction. The mitochondrial pro-survival protein Bcl-2 was upregulated, and antagonizing Bcl-2 function potentiated apoptosis induction by HBO. In conclusion, a single exposure to hyperbaric oxygenation induces lymphocyte apoptosis by a mitochondrial and not a Fas-related mechanism. Regulation of Fas and Bcl-2 may be regarded as protective measures of the cell in response to hyperbaric oxygen.
Item Type: |
Journal Article (Original Article) |
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Division/Institute: |
04 Faculty of Medicine > Department of Intensive Care, Emergency Medicine and Anaesthesiology (DINA) > Clinic and Policlinic for Anaesthesiology and Pain Therapy |
UniBE Contributor: |
Stüber, Frank |
Subjects: |
600 Technology > 610 Medicine & health |
ISSN: |
1360-8185 |
ISBN: |
19052874 |
Publisher: |
Springer |
Language: |
English |
Submitter: |
Factscience Import |
Date Deposited: |
04 Oct 2013 15:03 |
Last Modified: |
05 Dec 2022 14:19 |
Publisher DOI: |
10.1007/s10495-008-0280-z |
PubMed ID: |
19052874 |
Web of Science ID: |
000261954700009 |
BORIS DOI: |
10.48350/27304 |
URI: |
https://boris.unibe.ch/id/eprint/27304 (FactScience: 105948) |
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