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Prevention of hypoxia-induced cell death by Bcl-2 and Bcl-xL

Nature volume 374, pages 811–813 (1995)Cite this article

Abstract

THE proto-oncogene bcl-2, isolated from the t(14;18) chromosomal breakpoint in follicular B-lymphoma1–3, and abcl-2-related gene bcl-x (ref. 4) prevent apoptotic cell death induced by various treatments5–8. Although a mechanism has been proposed that involves Bcl-2 activity on reactive oxygen species (ROS)9,10, expression of Bcl-2 or Bcl-xL prevents cell death induced by withdrawal of oxygen (hypoxia), which drastically decreases the net formation of oxygen free radicals and does not increase oxidized lipid, protein or DNA. Furthermore, neither ROS scavenger nor inhibitor of ROS scavenger affects cell death, regardless of the expression of Bcl-2 or Bcl-xL. Thus our data suggest that Bcl-2 and Bcl-xL exert an anti-cell death function by a mechanism other than regulation of ROS activity.

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Author notes

  1. Shigeomi Shimizu

    Present address: 1st Department of Physiology, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka, 565, Japan

Authors and Affiliations

  1. Department of Surgery, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka, 565, Japan

    Shigeomi Shimizu, Wataru Kamiike & Hikaru Matsuda

  2. Department of Medical Genetics, Biomedical Research Center, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka, 565, Japan

    Yutaka Eguchi & Yoshihide Tsujimoto

  3. Department of Physiology, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka, 565, Japan

    Hiroaki Kosaka

Authors
  1. Shigeomi Shimizu
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  2. Yutaka Eguchi
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  3. Hiroaki Kosaka
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  4. Wataru Kamiike
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  5. Hikaru Matsuda
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  6. Yoshihide Tsujimoto
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Shimizu, S., Eguchi, Y., Kosaka, H. et al. Prevention of hypoxia-induced cell death by Bcl-2 and Bcl-xL. Nature 374, 811–813 (1995). https://doi.org/10.1038/374811a0

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