Faculty Research 1980 - 1989
Effect of DNA-damaging agents on isolated spleen cells and lung fibroblasts from the mouse mutant "wasted," a putative animal model for ataxia-telangiectasia.
Document Type
Article
Publication Date
1986
Keywords
Ataxia-Telangiectasia: me, Bleomycins, Disease-Models-Animal, DNA: bi, re, DNA-Repair, Fibroblasts: me, re, Gamma-Rays, In-Vitro, Lung: me, Mice, Mice-Mutant-Strains, Spleen: me, SUPPORT-NON-U-S-GOVT, SUPPORT-U-S-GOVT-P-H-S, 4-Nitroquinoline-1-Oxide
First Page
3979
Last Page
3982
JAX Source
Cancer-Res. 1986 Aug; 46(8):3979-82.
Grant
CA20408
Abstract
Spleen cells from control and wasted (wst) mice, a putative animal model for the human genetic disease ataxia-telangiectasia, were tested for inhibition of replicative (semiconservative) DNA synthesis after treatments with bleomycin, gamma-irradiation, 4-nitroquinoline 1-oxide, and ultraviolet irradiation. The wasted cells were found to be more resistant than control cells to the first three treatments, but equally sensitive to ultraviolet light. Bleomycin-stimulated repair synthesis in spleen cells was also studied by the CsCl/bromodeoxyuridine method and found to be similar in cells from wasted and control animals. Similarly, no differences in sensitivity to killing by gamma-rays, as manifested by relative cloning efficiencies, were demonstrated between primary lung fibroblasts from mutant and control mice. We concluded that observed defects in DNA repair in wasted cells are not identical to those reported in human cells from ataxia-telangiectasia patients.
Recommended Citation
Inoue T,
Aikawa K,
Tezuka H,
Kada T,
Shultz LD.
Effect of DNA-damaging agents on isolated spleen cells and lung fibroblasts from the mouse mutant "wasted," a putative animal model for ataxia-telangiectasia. Cancer-Res. 1986 Aug; 46(8):3979-82.