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Cellular oxygen toxicity. Oxidant injury without apoptosis
1CardioPulmonary Research Institute, State University of New York at Stony Brook School of Medicine, Mineola, New York 11501, USA.
The Journal of Biological Chemistry
|June 21, 1996
Summary
High oxygen levels (hyperoxia) can cause cell damage, but this study found it leads to necrosis, not apoptosis. Paradoxically, apoptosis occurs in lungs exposed to oxygen, suggesting it
Area of Science:
- Cellular Biology
- Toxicology
- Respiratory Medicine
Background:
- Aerobic life faces oxidative stress from molecular oxygen (O2).
- Antioxidant defenses can be overwhelmed by hyperoxia, leading to oxidative cell injury.
- Oxygen therapy, while life-saving, can cause lung injury due to reactive oxygen intermediates (ROI).
Purpose of the Study:
- To investigate the mechanism of cell death induced by hyperoxia.
- To determine if hyperoxia-induced cell death occurs via apoptosis or necrosis.
- To compare hyperoxia-induced cell death with that caused by specific ROI.
Main Methods:
- Cultured epithelial cells were exposed to 95% O2.
- Apoptosis was assayed using DNA-binding fluorescent dye, in situ end-labeling, and electron microscopy.
- Cell death mechanisms were compared between hyperoxia, hydrogen peroxide (H2O2), and superoxide anion (O2-).
Main Results:
- Hyperoxia induced cell death via necrosis, not apoptosis, in cultured epithelial cells.
- Lethal concentrations of H2O2 or O2- induced apoptosis.
- Apoptosis was observed in the lungs of animals exposed to 100% O2, contrasting with in vitro findings.
Conclusions:
- Oxygen toxicity mechanism is distinct from other oxidative injuries.
- Hyperoxia-induced cell death in vitro is primarily necrotic.
- Apoptosis observed in vivo during oxygen lung injury may not be a direct effect of hyperoxia.