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Programmed cell death and Bcl-2 protection in very low oxygen

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Abstract

PROGRAMMED cell death (PCD) is a fundamental feature of animal cells1, but the mechanism remains unknown. Similarly, the Bcl-2 oncoprotein can suppress PCD in a variety of cell types and circumstances2, 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 ROS3–6. 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.

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Authors and Affiliations

  1. MRC Developmental Neurobiology Programme, MRC Laboratory for Molecular Cell Biology and the Biology Department, University College London, London, WC1E 6BT, UK

    Michael D. Jacobson & Martin C. Raff

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  1. Michael D. Jacobson
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  2. Martin C. Raff
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Jacobson, M., Raff, M. Programmed cell death and Bcl-2 protection in very low oxygen. Nature 374, 814–816 (1995). https://doi.org/10.1038/374814a0

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  • DOI: https://doi.org/10.1038/374814a0

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