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Brilliant Fun 1 Pupil's Book by Charlotte Covill, Jeanne Perrett

By Charlotte Covill, Jeanne Perrett

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2 Adaptive response. , 1991; 1994). , 1994). There is inter-individual variability in the expression of the adaptive response; in one cytogenetic study 14/18 people exhibited a response (Bosi and Olivieri, 1989). At least for cytogenetic endpoints, there is a dose below which an adaptive response is not observed (Shadley and Wiencke, 1989). This of course suggests that the response, which is generally thought to reflect the induction of a repair system, requires a certain level of damage before it is induced; it follows from this that multiple radiation tracks are likely to be needed to induce the adaptive response in an exposed cell.

1995). The fact that high-LET radiation is significantly more mutagenic than low-LET radiation suggests that mds may have a high likelihood of producing mutations. This supports the hypothesis that multiple DNA lesions are more mutagenic than single lesions, and may explain why low-LET dose-response curves sometimes have a quadratic component. 5 Summary All types of mutations commonly seen in human cancers can be induced by ionizing radiation. These include point mutations and small deletions, as well as mutations arising at heterozygous loci by loss of heterozygosity.

3 DOSE-RESPONSE STUDIES WITH LOW-LET RADIATION / 43 Fig. 2. Mutagenicity of x rays at the HPRT locus in CHO cells. Cells are treated with the indicated dose of x rays, and HPRT mutants were character ized with the polymerase chain reaction. 4 multi-locus alterations including both deletions and recombination events) mutants with linear kinetics. In Tk6 human lymphoblast cells, thymidine kinase mutants also arise mainly from loss of heterozyosity resulting from a combination of deletions and recombination events.

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