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Title: Repair of chromosome damage induced by X-irradiation during G2 phase in a line of normal human fibroblasts and its malignant derivative

Abstract

A line of normal human skin fibroblasts (KD) differed from its malignant derivative (HUT-14) in the extent of cytogenetic damage induced by X-irradiation during G2 phase. Malignant cells had significantly more chromatid breaks and gaps after exposure to 25, 50, or 100 rad. The gaps may represent single-strand breaks. Results from alkaline elution of cellular DNA immediately after irradiation showed that the normal and malignant cells in asynchronous population were equally sensitive to DNA single-strand breakage by X-irradiation. Caffeine or beta-cytosine arabinoside (ara-C), inhibitors of DNA repair, when added directly following G2 phase exposure, significantly increased the incidence of radiation-induced chromatid damage in the normal cells. In contrast, similar treatment of the malignant cells had little influence. Ara-C differed from caffeine in its effects; whereas both agents increased the frequency of chromatid breaks and gaps, only ara-C increased the frequency of gaps to the level observed in the irradiated malignant cells. Addition of catalase, a scavenger of the derivative free hydroxyl radical (.OH), to the cultures of malignant cells before, during, and following irradiation significantly reduced the chromatid damage; and catalase prevented formation of chromatid gaps. The DNA damage induced by X-ray during G2 phase in the normal KD cellsmore » was apparently repaired by a caffeine- and ara-C-sensitive mechanism(s) that was deficient or absent in their malignant derivatives.« less

Authors:
; ; ; ;
Publication Date:
Research Org.:
Department of Pathology, Howard University College of Medicine, Washington, DC
OSTI Identifier:
6654578
Resource Type:
Journal Article
Journal Name:
J. Natl. Cancer Inst.; (United States)
Additional Journal Information:
Journal Volume: 69:2
Country of Publication:
United States
Language:
English
Subject:
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.; 62 RADIOLOGY AND NUCLEAR MEDICINE; CHROMOSOMES; BIOLOGICAL RADIATION EFFECTS; FIBROBLASTS; RADIOSENSITIVITY; BIOLOGICAL REPAIR; CELL CYCLE; CHROMOSOMAL ABERRATIONS; DNA; RADIATION DOSES; RADIOSENSITIVITY EFFECTS; RESPONSE MODIFYING FACTORS; X RADIATION; ANIMAL CELLS; BIOLOGICAL EFFECTS; BIOLOGICAL RECOVERY; CONNECTIVE TISSUE CELLS; DOSES; ELECTROMAGNETIC RADIATION; IONIZING RADIATIONS; MUTATIONS; NUCLEIC ACIDS; ORGANIC COMPOUNDS; RADIATION EFFECTS; RADIATIONS; RECOVERY; REPAIR; SOMATIC CELLS; 560121* - Radiation Effects on Cells- External Source- (-1987); 550603 - Medicine- External Radiation in Therapy- (1980-)

Citation Formats

Parshad, R, Gantt, R, Sanford, K K, Jones, G M, and Tarone, R E. Repair of chromosome damage induced by X-irradiation during G2 phase in a line of normal human fibroblasts and its malignant derivative. United States: N. p., 1982. Web.
Parshad, R, Gantt, R, Sanford, K K, Jones, G M, & Tarone, R E. Repair of chromosome damage induced by X-irradiation during G2 phase in a line of normal human fibroblasts and its malignant derivative. United States.
Parshad, R, Gantt, R, Sanford, K K, Jones, G M, and Tarone, R E. 1982. "Repair of chromosome damage induced by X-irradiation during G2 phase in a line of normal human fibroblasts and its malignant derivative". United States.
@article{osti_6654578,
title = {Repair of chromosome damage induced by X-irradiation during G2 phase in a line of normal human fibroblasts and its malignant derivative},
author = {Parshad, R and Gantt, R and Sanford, K K and Jones, G M and Tarone, R E},
abstractNote = {A line of normal human skin fibroblasts (KD) differed from its malignant derivative (HUT-14) in the extent of cytogenetic damage induced by X-irradiation during G2 phase. Malignant cells had significantly more chromatid breaks and gaps after exposure to 25, 50, or 100 rad. The gaps may represent single-strand breaks. Results from alkaline elution of cellular DNA immediately after irradiation showed that the normal and malignant cells in asynchronous population were equally sensitive to DNA single-strand breakage by X-irradiation. Caffeine or beta-cytosine arabinoside (ara-C), inhibitors of DNA repair, when added directly following G2 phase exposure, significantly increased the incidence of radiation-induced chromatid damage in the normal cells. In contrast, similar treatment of the malignant cells had little influence. Ara-C differed from caffeine in its effects; whereas both agents increased the frequency of chromatid breaks and gaps, only ara-C increased the frequency of gaps to the level observed in the irradiated malignant cells. Addition of catalase, a scavenger of the derivative free hydroxyl radical (.OH), to the cultures of malignant cells before, during, and following irradiation significantly reduced the chromatid damage; and catalase prevented formation of chromatid gaps. The DNA damage induced by X-ray during G2 phase in the normal KD cells was apparently repaired by a caffeine- and ara-C-sensitive mechanism(s) that was deficient or absent in their malignant derivatives.},
doi = {},
url = {https://www.osti.gov/biblio/6654578}, journal = {J. Natl. Cancer Inst.; (United States)},
number = ,
volume = 69:2,
place = {United States},
year = {Sun Aug 01 00:00:00 EDT 1982},
month = {Sun Aug 01 00:00:00 EDT 1982}
}