Cancer Research Infection and Cancer: Biology, Therapeutics, and Prevention  Cancer Health Disparities Conference 2009
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online

[Cancer Research 46, 1703-1706, April 1, 1986]
© 1986 American Association for Cancer Research

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Fornace, A. J.
Right arrow Articles by Mitchell, J. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fornace, A. J., Jr.
Right arrow Articles by Mitchell, J. B.

Repair of Ionizing Radiation DNA Base Damage in Ataxia-Telangiectasia Cells

Albert J. Fornace, Jr.1, Timothy J. Kinsella, Patricia P. Dobson and James B. Mitchell

Radiobiology Section, Radiation Oncology Branch, Clinical Oncology Program, Division of Cancer Treatment, National Cancer Institute, NIH, Bethesda, Maryland 20892

Micrococcus luteus endonuclease sensitive sites were measured by alkaline elution in normal human and ataxia-telangiectasia (AT) fibroblasts after ionizing radiation. Due to the sensitivity of this assay, repair of base damage after 3 to 6 kilorads has been measured after oxic or hypoxic radiation. With 5.5 kilorads of oxic radiation, more than 50% of the base damage was removed after 1.5 h of repair incubation in all cells, including exr+ and exr- AT cells, and approximately 75% was removed by 4 h. After 3 or 4.5 kilorads of hypoxic X-irradiation, repair was equivalent in normal and exr- AT cells. This study included three exr- AT strains which have been reported to be deficient in the removal of {gamma}-ray base damage at higher doses. Since these strains repaired ionizing radiation base damage normally at lower doses, which are more relevant to survival, it is concluded that the X-ray hypersensitivity of AT cells is probably not related to the repair of base damage.

1 To whom requests for reprints should be addressed, at National Cancer Institute/NIH, Radiation Oncology Branch, Building 10, Room B3B69, 9000 Rockville Pike, Bethesda, MD 20892.

Received 6/28/85. Revised 12/16/85. Accepted 12/30/85.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1986 by the American Association for Cancer Research.