Modifiers of Radiation-Induced Apoptosis

EL4 murine lymphoma cells and F9 murine teratocarcinoma cells undergo apoptosis-like cell death after exposure to ionizing radiation. Apoptosis differs in several ways from classical clonogenic cell killing by radiation. We have tested several modifiers and radiomimetic agents in an effort to determ...

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Bibliographic Details
Published in:Radiation research 1993-12, Vol.136 (3), p.320-326
Main Authors: Langley, Ruth E., Palayoor, Sanjeewani T., Coleman, C. Norman, Bump, Edward A.
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Apoptosis - radiation effects
Biological and medical sciences
Biological effects of radiation
Cell death
Cell lines
Cellular differentiation
DNA - metabolism
DNA damage
DNA fragmentation
Embryonal Carcinoma Stem Cells
Fundamental and applied biological sciences. Psychology
Hydrogen Peroxide - metabolism
Ionizing radiation
Ionizing radiations
Irradiation
Lipid Peroxidation
Lymphoma - pathology
Mice
Neoplastic Stem Cells - pathology
Nucleosomes - metabolism
Radiation damage
Stem cells
Symposium: Apoptosis/Programmed Cell Death
Teratocarcinoma - pathology
Tissues, organs and organisms biophysics
Tumor Cells, Cultured
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Summary:EL4 murine lymphoma cells and F9 murine teratocarcinoma cells undergo apoptosis-like cell death after exposure to ionizing radiation. Apoptosis differs in several ways from classical clonogenic cell killing by radiation. We have tested several modifiers and radiomimetic agents in an effort to determine if the mechanism of induction of apoptosis by radiation differs from the mechanism of classical clonogenic cell killing by radiation, and consequently that these two end points of radiation action might be differentially modifiable. We found that internucleosomal DNA fragmentation, characteristic of apoptosis, can result from treatment of EL4 and F9 cells with agents that have diverse modes of action: tert-butyl hydroperoxide, diazenedicarboxylic acid bis(N,N-piperidide), and etoposide. Hydrogen peroxide did not induce internucleosomal DNA fragmentation at concentrations expected to be produced by the doses of ionizing radiation that we used. Radiation-induced DNA fragmentation could be inhibited by 3-aminobenzamide, dibutryl cyclic AMP, or 4-hydroxy-2,2,6,6,-tetramethylpiperidine-N-oxyl, although in this respect there appear to be marked differences between the cell lines.
ISSN:0033-7587
1938-5404
DOI:10.2307/3578543