THE role of chromatid exchange in the origin of chromosome aberrations has been a subject of research since the chromatid exchange hypothesis of chromosome aberrations was proposed1. Which of the breakage–treunion hypothesis2 and the exchange hypothesis better explains the origin of chromosome aberrations is still disputed3,4. The part played by DNA repair in aberration and exchange formation has been identified5,6, and there is much evidence for non-random distribution of chromosome aberrations, especially in the heterochromatic regions7,8. We have shown previously by autoradiography, that sister chromatid exchanges (SCEs) induced by 7,12-dimethylbenz(a)anthracene (DMBA) are frequently associated with aberrations8. Newly introduced 5-bromodeoxyuridine(BUdR)–33258 Hoechst methods for SCEs9,10 have made it possible to reanalyse these problems in more detail and with considerable accuracy. The results presented here indicate that two different hydrocarbon carcinogens, DMBA and 7,8,12-trimethylbenz(a)-anthracene (TMBA), induce aberrations localised in the same chromosomal regions of the rat bone marrow cells and that the targets for chromosome aberrations and for SCE are identical; in other words, both phenomena are related.
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About this article
Sister chromatid exchanges in human bone marrow cells I. Control subjects and patients with leukaemia
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