Abstract
Programmed cell death (PCD) is a fundamental feature of animal cells, but the mechanism remains unknown. Similarly, the Bcl-2 oncoprotein can suppress PCD in a variety of cell types and circumstances, but it is not known how it does so. It has been suggested that PCD involves the generation of reactive oxygen species (ROS) and that Bcl-2 protects against PCD by inhibiting the generation or action of ROS. To determine whether ROS are required for PCD, we cultured cells in a near-anaerobic atmosphere where the generation of ROS would be expected not to occur, or at least to be greatly reduced. We find that these conditions inhibit PCD induced by ROS-generating agents but do not inhibit PCD induced by other means. Furthermore, we show that Bcl-2 can protect cells from PCD in these anaerobic conditions. These results suggest that ROS are not required for PCD, and that Bcl-2 protects against PCD in ways that do not depend on the inhibition of ROS production or activity.
Keywords
Reactive oxygen speciesProgrammed cell deathCell biologyApoptosisCellChemistryBiologyBiochemistry
MeSH Terms
AlkaloidsAntigensSurfaceAntioxidantsApoptosisCell LineTransformedHumansInterleukin-3Lipid PeroxidationOxygenProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2Reactive Oxygen SpeciesStaurosporinefas Receptor
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Publication Info
- Year
- 1995
- Type
- article
- Volume
- 374
- Issue
- 6525
- Pages
- 814-816
- Citations
- 630
- Access
- Closed
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Cite This
Michael D. Jacobson,
Martin Raff
(1995).
Programmed cell death and Bcl-2 protection in very low oxygen.
Nature
, 374
(6525)
, 814-816.
https://doi.org/10.1038/374814a0
Identifiers
- DOI
- 10.1038/374814a0
- PMID
- 7536895