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CHAPTER 28 



cells that divide as occur in nondividing 

 cells, but in this case, aneuploidy can result 

 following nuclear division (recall the discus- 

 sion of aneuploidy in Chapters 18 and 19). 

 In dividing cells, most of the phenotypic 

 damage is the result of aneuploidy, and most 

 of this is the consequence of single break- 

 ages that fail to restitute, at least for those 

 mutation-inducing agents which are capable of 

 breaking chromosomes. (It may be noted 

 that all known agents that increase the point 

 mutation rate also break chromosomes.) 



We should not consider the preceding dis- 

 cussion of the somatic effects of mutation as 

 a digression from the main aims of this Chap- 

 ter, because such cells actually comprise a 

 population which has been produced by asex- 

 ual reproduction (cell division). Let us now 

 consider, in a general way, the consequences 

 of increasing the frequency of mutations in the 

 human germ line. The earlier that mutation 

 occurs in the germ line, the greater will be 

 the portion of all germ cells produced which 

 carry the mutant. Of course, the upper 

 hmit of gametes carrying a particular induced 

 mutant is usually 50 per cent. Consider the 

 effect of exposing the gonads to manmade 

 high-energy radiation (Figure 28-3). Before 

 the exposure to manmade radiation, the load 

 of mutants is presumably at equilibrium, the 

 rate of origin of mutants equaling the rate 

 of their loss via genetic death. Starting with 

 the first generation to receive the additional 

 radiation exposure, the mutant load increases 

 each generation until a new equilibrium is 

 reached. At that point the higher number 



GENETIC 

 LOAD 



of genetic deaths will equal the higher num- 

 ber of new mutants. If at some still later 

 generation, the extra radiation exposure 

 ceased, the mutational load would decrease 

 gradually (because of variations in persist- 

 ence) via genetic deaths, until the old equilib- 

 rium were reached once again. 



It has become very important to learn in 

 detail the genetic effects of high-energy radia- 

 tion to which human populations are being 

 subjected either purposely or circumstan- 

 tially. In order to make the best evaluation, 

 we would like to know, among other things, 

 the precise way in which the energy of various 

 radiations is distributed in tissue, the exact 

 amount of gonadal exposure to radiations of 

 different types, the kinds and frequencies of 

 the different types of mutation each of these 

 radiations would produce in the different 

 stages of gametogenesis in males and in fe- 

 males, the detriment of the induced mutants 

 in hetero- and homozygous condition, the 

 exact proportions of all mutants that are 

 heterotic, and their amount of heterosis, as 

 well as the persistence of these mutants. We 

 certainly do not have, at present, as much 

 information about any one of these factors 

 as we would like to have, but available in- 

 formation along these lines can already give 

 us approximate answers (see references at 

 the end of this Chapter). In the discussion 

 following, it should be realized, therefore, 

 that all figures used may be in error by as 

 much as a factor of two or more. 



It has been a practice to discuss the germ 

 line effect of radiation in terms of the amount 



FIGURE 28-3. Genetic load 

 and exposure to radiation. 



K 



Radiation _ { 

 Exposure \ 



GENERATIONS 



