Jacobson M D, Raff M C
MRC Developmental Neurobiology Programme, MRC Laboratory for Molecular Cell Biology, University College London, UK.
Nature. 1995 Apr 27;374(6525):814-6. doi: 10.1038/374814a0.
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.
程序性细胞死亡（PCD）是动物细胞的一个基本特征，但其机制仍然未知。同样，Bcl-2癌蛋白可以在多种细胞类型和情况下抑制PCD，但尚不清楚其具体作用方式。有人提出，PCD涉及活性氧（ROS）的产生，而Bcl-2通过抑制ROS的产生或作用来保护细胞免受PCD。为了确定ROS是否是PCD所必需的，我们在近乎厌氧的环境中培养细胞，在这种环境中预计不会产生ROS，或者至少会大大减少。我们发现这些条件抑制了由ROS生成剂诱导的PCD，但不抑制由其他方式诱导的PCD。此外，我们表明Bcl-2可以在这些厌氧条件下保护细胞免受PCD。这些结果表明，PCD不需要ROS，并且Bcl-2以不依赖于抑制ROS产生或活性的方式保护细胞免受PCD。
