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Abstract

In agreement with our earlier observation (Scott and Zampetti-Bosseler, 1982) on X-irradiated normal and ataxia-telangiectasia (A-T) fibroblasts, we now report that after bleomycin or neocarzinostatin treatment also, A-T cells exhibit less G-2 delay than normal cells. We confirm that A-T cells sustain more chromosome damage and lethality than normal cells after bleomycin. These observations support the hypothesis (Painter and Young, 1980) that A-T cells are defective in the recognition of certain lesions which normally lead to delays in progression through the cell cycle, during which they are repaired, and which, if unrepaired, lead to cell lethal chromosome damage. However, we find that after bleomycin, as opposed to X-rays, the contribution of this type of lesion to cell death is minimal. The predominant lesions leading to cell death after bleomycin are not manifested at chromosome aberrations and do not lead to G-2 delay or DNA synthesis inhibition. A-T cells are defective in the recognition and/or repair of both types of lesion.

Additional information

Authors: ZAMPETTI BOSSELER F UNIVERSITE LIBRE DE BRUXELLES (BELGIUM) SCOTT D PATERSON LABORATORIES, CHRISTIE HOSPITAL AND HOLT RADIUM INSTITUTE, MANCHESTER (UK) , UNIVERSITE LIBRE DE BRUXELLES (BELGIUM);PATERSON LABORATORIES, CHRISTIE HOSPITAL AND HOLT RADIUM INSTITUTE, MANCHESTER (UK)
Bibliographic Reference: MUTATION RESEARCH, VOL. 151 (1985), PP. 89-94
Record Number: 1989124019500 / Last updated on: 1987-01-01
Category: PUBLICATION
Available languages: en