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[Analysis of DNA damage and mutations induced by radon daughter products] [electronic resource].

Published:
Washington, D.C. : United States. Dept. of Energy, 1992.
Oak Ridge, Tenn. : Distributed by the Office of Scientific and Technical Information, U.S. Dept. of Energy.
Physical Description:
Pages: (11 pages) : digital, PDF file
Additional Creators:
United States. Department of Energy and United States. Department of Energy. Office of Scientific and Technical Information
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Summary:
In order to understand the genetic and somatic risks associated with exposure to radon and its daughter products, it is important to characterize those lesions that lead to mutation induction and carcinogenesis. The effect of exposure to the radon daughter (212)Bi has been analyzed in 4 CHO cell lines, CHO-KL, xrs-5, AA8 and EM9. These cell lines have different radiation sensitivities and different abilities to rejoin radiation-induced DNA strand breaks. Three endpoints have been examined in these cells; cell killing, chromosome aberration induction and mutation induction. We find RBEs for AA8, EM9 and CHO-KL of about 2.5-4 for cell killing and around 2 for G2-induced aberrations. The RBEs for xrs-5 cells are much smaller for cell killing and chromosome aberration induction, suggesting that the principle lethal lesion resulting from [212]Bi exposure is a non-repaired DNA double-strand break. (The CHO cell line xrs-5 is defective in the rejoining of DNA double-strand breaks.) The survival curves suggest that a portion of the cell killing is probably derived from the low LET beta component of the radiation. Mutation studies suggest that while the lethal and pre-mutagenic lesions might overlap, they are not exactly the same. RBEs for gene mutation induction in AA8 and EM9 cells are higher than the RBEs for killing and chromosome aberration induction. Interestingly, CHO-KL is not more sensitive to mutation induction than killing or chromosome aberration induction by [212]Bi suggesting that this cell line differs from AA8 and EM9 in its ability to repair a premutagenic lesion induced by [212]Bi. These studies should help define the nature of the lesions induced by radon exposure and thereby help understand the carcinogenic risk from radon exposure and how it differs from low LET radiation exposure.
Report Numbers:
E 1.99:doe/er/60661-2
doe/er/60661-2
Subject(s):
Other Subject(s):
Note:
Published through SciTech Connect.
01/01/1992.
"doe/er/60661-2"
"DE93007141"
Chicago Univ., IL (United States)
Funding Information:
FG02-88ER60661
View MARC record | catkey: 14793950