Heterogeneity in the Clastogenic Response to X-Rays in Lymphocytes from Ataxia-Telangiectasia Heterozygotes and Controls
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1992/05/01
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Description:A coded analysis of X-ray-induced chromatid aberrations in lymphocyte cultures from 45 control individuals and 19 ataxia-telangiectasia (A-T) heterozygotes was performed. The distribution of chromatid breaks induced in the late G2 portion of the cell cycle by 60 cGy of X-rays appeared bimodal in the study population. In six controls (13 percent) and in 12 of 19 (63 percent) A-T heterozygotes, the yields of X-ray-induced breaks observed were within the higher mode of the distribution. However, lymphocytes from A-T heterozygotes sensitive to the induction of chromatid breaks by 60 cGy did not contain increased numbers of aberrations following exposure to 20 cGy. The radio-resistant inhibition of DNA synthesis that occurs in A-T homozygotes was not observed in heterozygotes. Co-cultivation experiments showed an increased G2 delay in lymphocytes from an A-T heterozygote whose lymphocytes contained increased X-ray-induced chromatid breaks. The results show a significant association of A-T heterozygosity with G2 chromosomal sensitivity (P less than 0.001; Wilcoxon rank sum test). The measurement of X-ray-induced breaks, however, failed to identify 37 percent of A-T heterozygotes tested. The predicted prevalence of increased sensitivity to X-rays in controls is approximately three- to 30-fold greater than the estimated frequency of A-T heterozygotes in the general population. Therefore, although the increased sensitivity to X-ray-induced chromatid breaks appears to be associated with the A-T-gene, it is not a reliable indicator of A-T heterozygosity. Genetic or environmental factors other than the A-T gene also must be involved in the increased clastogenic response. [Description provided by NIOSH]
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ISSN:0957-5243
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Pages in Document:237-245
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Volume:3
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Issue:3
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NIOSHTIC Number:nn:20000997
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Citation:Cancer Causes Control 1992 May; 3(3):237-245
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Contact Point Address:Department of Epidemiology and Biostatistics, School of Medicine, University of California, San Francisco 94143
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Federal Fiscal Year:1992
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Performing Organization:Harvard University, School of Public Health, Occupational Health Program, Boston, Massachusetts
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Peer Reviewed:True
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Start Date:19910930
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Source Full Name:Cancer Causes and Control
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End Date:19940929
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Main Document Checksum:urn:sha-512:47fcaddc317e6c07c089ff89c084f805c71a3d1714c3e06e4b82eb3c97f3a0436b60ab8d80295fc85d4605f13100c82a3aaa1b4ce7b33771726aecd050e54a29
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