Related Experiment Video
Updated: Jun 27, 2026
13:20
Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro
Published on: July 17, 2018
Hyperbaric oxygen induces apoptosis via a mitochondrial mechanism
Stefan U Weber1, Andreas Koch, Jens Kankeleit
1Department of Anesthesiology and Intensive Care Medicine, University of Bonn Medical Center, Sigmund Freud Str. 25, 53105 Bonn, Germany. Stefan.weber@ukb.uni-bonn.de
Apoptosis : an International Journal on Programmed Cell Death
|December 5, 2008
Summary
Hyperbaric oxygenation triggers lymphocyte apoptosis via a mitochondrial pathway, not the Fas receptor. Bcl-2 upregulation suggests a cellular protective response to this oxygen therapy.
Area of Science:
- Cell Biology
- Oxygen Toxicity
- Immunology
Background:
- Therapeutic hyperbaric oxygenation (HBO) involves exposing cells to elevated oxygen levels.
- Lymphocytes are particularly susceptible to oxidative stress under hyperbaric conditions.
- Understanding the mechanisms of HBO-induced cell death is crucial for optimizing treatment protocols.
Purpose of the Study:
- To elucidate the specific molecular mechanisms by which hyperbaric oxygen induces apoptosis in lymphocytes.
- To differentiate between the roles of the mitochondrial pathway and the Fas-related pathway in HBO-induced lymphocyte apoptosis.
Main Methods:
- Jurkat-T cells were exposed to varying hyperbaric oxygen pressures (1-3 atmospheres) for different durations (0.5-4 hours).
- Apoptosis was assessed using phosphatidylserine externalization, caspase-3 activation, and DNA fragmentation assays via flow cytometry.
- Mitochondrial membrane potential, caspase-9, caspase-8, Fas, and Bcl-2 expression levels were analyzed.
Main Results:
- Hyperbaric oxygenation induced significant lymphocyte apoptosis within 30 minutes.
- Fas receptor expression was downregulated, while caspase-9 activation and mitochondrial membrane potential loss were observed.
- Inhibition of caspase-9, but not caspase-8, blocked HBO-induced apoptosis.
- Upregulation of the anti-apoptotic protein Bcl-2 was noted, and its inhibition enhanced HBO-induced apoptosis.
Conclusions:
- Hyperbaric oxygenation induces lymphocyte apoptosis primarily through a mitochondrial-dependent pathway.
- The Fas death receptor pathway is not the primary mediator of HBO-induced lymphocyte apoptosis.
- Upregulation of Bcl-2 and downregulation of Fas suggest cellular adaptive responses to mitigate HBO-induced damage.
Related Concept Videos
01:31The Intrinsic Apoptotic Pathway
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
01:30Apoptosis
Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
01:17The Extrinsic Apoptotic Pathway
The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
01:00Cellular Injury I: Introduction
Cellular injury occurs when a cell cannot maintain homeostasis or adapt to stressors such as hypoxia, toxins, or trauma. Depending on severity and duration, injury may be reversible, allowing recovery, or irreversible, leading to cell death.General Mechanisms of Cell InjuryAlthough causes vary, most cellular injuries arise from a few key mechanisms that disrupt essential functions and often amplify one another. Cell survival depends on the extent and balance of these disturbances.ATP depletion...
01:18Autophagic Cell Death
Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
01:22Cellular Injury V: Apoptosis and Autophagy
Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...