Abstract
The ability of UV light, mitomycin C and ionizing radiation to induce the formation of sister chromatid exchanges (SCEs) at the same locus in successive cell generations was investigated in human lymphocytes. Cells were exposed to the DNA damaging agents after they had completed their first round of DNA replication, and SCEs were examined at the third division in chromosomes that had been differentially stained three ways. Although some of these treatments induced long-lived lesions that increased the frequency of SCEs in successive cell generations, none of the lesions led to the formation of consecutive SCEs at the same locus in successive cell generations. This observation seriously challenges the hypothesis that SCE cancellation results as a consequence of persistence of the lesions induced by these agents.
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References
Biegel JA, Conner MK, Boggs SS (1982) Cellular replication kinetics and persistence of sister chromatid exchange-inducing lesions in normal and lymphoma AKR cells following exposure to 1,3-bis-(2-chloroethyl)-1-nitrosourea. Cancer Res 42:2816–2820
Conner MK, Cheng M (1983) Sister chromatid exchanges induced in murine alveolar macrophage and bone marrow cells in vivo following various ethyl carbamate treatment protocols. Cancer Res 43:965–971
Conner MK, Luo JE, Gotera OG (1983) Induction of sister chromatid exchanges in multiple murine tissues in vivo by diepoxybutane administered by various protocols. Mutat Res 108:251–263
Conner MK, Cheng M, Biegel JA (1984) A path probability model for sister chromatid exchanges induced by alkylating agents. Mutat Res 126:35–46
Djordjevic B, Szybalski W (1960) Genetics of human cell lines. III. Incorporation of 5-bromo- and 5-iododeoxyuridine into the deoxyribonucleic acid of human cells and its effects on radiation sensitivity. J Exp Med 112:509–531
Gutiérrez C, Schvartzman JB, López-Sáez JF (1981) Effect of growth temperature on the formation of sister chromatid exchange in BrdUrd-substituted chromosomes. Exp Cell Res 134:73–79
Ishii Y, Bender MA (1978) Factors influencing the frequency of mitomycin C-induced sister chromatid exchanges in 5-bromodeoxyuridine-substituted human lymphocytes in culture. Mutat Res 51:411–418
Ishii Y, Bender MA (1980) Effects of inhibitors of DNA synthesis on spontaneous and ultraviolet light-induced sister chromatid exchanges in Chinese hamster cells. Mutat Res 79:19–32
Kato H (1973) Induction of sister chromatid exchanges by UV light and its inhibition by caffeine. Exp Cell Res 82:383–390
Lindenhahn M, Schubert I (1983) On the origin of hydroxyureainduced chromatid aberrations in G2 chromosomes with BrdUrd in only one of the sister chromatids. Mutat Res 108:301–316
Littlefield LG, Colyer SP, Joiner EE, DuFrain RJ (1979) Sister chromatid exchanges in human lymphocytes exposed to ionizing radiation during G0- Radiat Res 78:514–521
O'Neill JP, Heartlein MW, Preston RJ (1983) Sister chromatid exchanges and gene mutations are induced by the replication of 5-bromo- and 5-chlorodeoxyuridine-substituted DNA. Mutat Res 109:259–270
Perry P, Evans HJ (1975) Cytological detection of mutagen-carcinogen exposure by sister chromatid exchange. Nature 258:121–125
Renault G, Gentil A, Chouroulinkov I (1982) Kinetics of induction of sister chromatid exchange by X rays through two cell cycles. Mutat Res 94:359–368
Sandberg AA (1982) Sister chromatid exchange. Alan R Liss, New York, p 706
Schvartzman JB (1979) Three-way differentiation of sister chromatids in 5-bromodeoxyuridine-substituted chromosomes. J Hered 70:423–424
Schvartzman JB, Goyanes VJ (1980) A new method for the identification of SCEs per cell cycle in BrdUrd-substituted chromosomes. Cell Biol Int Rep 4:415–423
Schvartzman JB, Gutiérrez C (1980) The relationship between the cell time available for repair and the effectiveness of a damaging treatment in provoking the formation of sister chromatid exchanges. Mutat Res 72:483–489
Schvartzman JB, Goyanes VJ, Tice RR (1984) DNA damage persistence and site specificity in SCE formation. In: Tice RR, Hollaender A (eds) Sister chromatid exchange: 25 years of experimental research. Plenum, New York, pp 215–227
Shaffer DA (1977) Replication bypass model of sister chromatid exchanges and implications for Bloom's syndrome and Fanconi's anemia. Hum Genet 39:177–190
Stetka DG (1979) Further analysis of the replication bypass model for sister chromatid exchange. Hum Genet 49:63–69
Stetka DG, Spahn MC (1984) SCEs are induced by replication of BrdU-substituted DNA templates, but not by incorporation of BrdU into nascent DNA. Mutat Res 140:33–42
Tice RR, Hollaender A (1984) Sister chromatid exchange: 25 years of experimental research. Plenum, New York
Tice RR, Schvartzman JB (1982) Sister chromatid exchange: A measure of DNA damage persistence. In: Sandberg AA (ed) Sister chromatid exchange. Alan R Liss, New York, pp 33–45
Wolff S (1982) Sister chromatid exchange. John Wiley, New York p 306
Wolff S, Bodycote J, Painter RB (1974) Sister chromatid exchanges induced in Chinese hamster cells by UV irradiation at different stages of the cell cycle: The necessity for cells to pass through S. Mutat Res 25:73–81
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Schvartzman, J.B., Goyanes, V.J., Campos, A. et al. Persistence of DNA lesions and the cytological cancellation of sister chromatid exchanges. Chromosoma 92, 7–10 (1985). https://doi.org/10.1007/BF00327239
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DOI: https://doi.org/10.1007/BF00327239