Abstract

It was found several years ago (1) that, immediately after a large, single dose of X-rays to young mice, the chromosome aberrations in liver cells increase to become as high as 90 %. Thereafter the percentage decreases slowly over a period of many months to reach control levels after a year or more. The question immediately arose as to why the aberrations declined. The immediate explanation for this was that the cells of the liver normally undergo cell division very rarely, and estimates seemed to indicate that the mitotic rate would be about sufficient to account for the decrease, provided that each aberrant cell died on attempting cell division and was replaced by the division of a normal cell. This explanation was quite satisfying until data became available on mice irradiated with neutrons (2). Here the aberration frequency immediately jumps to very high values and remains as high as the initial values for at least 14 months. If the cell division hypothesis operates for the X-ray case, it surely should operate for the neutron case as well. Since it does not, one is tempted to brand the hypothesis as untenable and look for another. There is, however, a good deal of evidence indicating that cells with aberrant chromosomes are indeed eliminated by cell division. The phenomenon is continually seen in plant cells and in cells in tissue culture. Further, chromosome aberrations increase steadily with age in liver cells (1), whereas in bone marrow cells they do not (3). Since bone marrow cells are certainly as sensitive as liver cells, it seems almost axiomatic that the aberrations in bone marrow cells are eliminated by cell division but that insufficient cell division takes place in liver to eliminate the spontaneously formed aberrations. There is thus an apparent contradiction, and it would seem wise to look for alternative explanations. One such explanation would be that the chromosomes can

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