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Cell death is an important physiological process, but it can be triggered by both physiological and nonphysiological stimuli. The product of the bcl-2 gene has the ability to inhibit a physiological cell death process that can be activated by a variety of physiological signals, such as growth factor deprivation. This report describes the use of electron microscopy to examine the effects of two cytotoxic drugs on factor-dependent cells that constitutively express the human bcl-2 gene. Although all cells treated with sodium azide showed changes typical of necrosis, in the absence of Bcl-2 the cells died more rapidly and also displayed features of apoptosis. The fact that Bcl-2 could delay cell death argues that cells can activate internal cell death mechanisms to commit suicide before they are killed by a cytotoxin. Northern analysis showed that growth factor did not preserve viability of the cells through induction of bcl-2. However, growth factor may prevent activation of the physiological cell death mechanisms that bcl-2 can control. This process may constitute a primitive defense response, and blocking it may provide a means of limiting damage caused by otherwise sublethal injuries.

Original publication

DOI

10.1002/(SICI)1097-0029(19960615)34:3<259::AID-JEMT8>3.0.CO;2-K

Type

Journal article

Journal

Microsc Res Tech

Publication Date

15/06/1996

Volume

34

Pages

259 - 266

Keywords

Animals, Apoptosis, Azides, Blotting, Northern, Bone Marrow, Bone Marrow Cells, Cell Cycle, Cell Line, Colchicine, Gene Expression Regulation, Humans, Mice, Microscopy, Electron, Mutagens, Necrosis, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-bcl-2, Sodium Azide