DNA crosslinking, sister-chromatid exchange and specific-locus mutations |
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Authors: | A V Carrano L H Thompson D G Stetka J L Minkler J A Mazrimas S Fong |
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Affiliation: | Biomedical Sciences Division, L-452, Lawrence Livermore Laboratory, Livermore, CA 94550 U.S.A. |
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Abstract: | Chinese hamster ovary cells were treated with the DNA-crosslinking chemicals, mitomycin C (MMC) and porfiromycin (POR), and their monofunctional derivative decarbamoyl mitomycin C (DCMMC). After exposure, the cells were studied for the induction of sister-chromatid exchanges (SCEs) and mutations at the hypoxanthine phosphoribosyltransferase and adenine phosphoribosyltransferase loci. The frequency of SCEs varied significantly in successive sampling intervals, requiring the weighting of each interval by the percentage of second-division mitosis in that interval to obtain the mean SCE frequency for each dose. All 3 compounds were potent inducers of SCEs but weakly mutagenic. All 3 chemicals by concentration were approximately equally effective in inducing SCEs or mutations. When the induced SCEs and mutations were compared at equal levels of survival, DCMMC was slightly more effective than MMC or POR in inducing SCEs and somewhat less mutagenic. These results indicate that the DNA interstrand crosslink is not the major lesion responsible for the induction of SCE or mutation by these compounds. |
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Keywords: | AA 8-aza-adenine resistance to aza-adenine AG 8-azaguanine resistance to azaguanine APRT adenine phosphoribosyltransferase Brd Urd 5-bromodeoxyuridine CHO Chinese hamster ovary DCMMC decarbamoyl mitomycin C EDTA ethylene-diaminetetra-acetic acid HAP hydroxyapatite HPRT hypoxanthine phosphoribosyltransferase MMC mitomycin C POR porfiromycin SCE sister-chromatid exchange TdR deoxyribose thymidine TG 6-thioguanine XP xeroderma pigmentosum |
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