MECHANISMS OF LIFE-SPAN SHORTENING 241 



even of deficiencies of chromosome parts that causes the somatic damage, but 

 the loss of the entire chromosome, referable to its breakage. For the chromo- 

 some having a small deficiency would in these cases have afforded protection 

 against all point-mutations and small deficiencies in the other member of the 

 pair except those located in the very same small region as it itself occupied. 

 On the other hand, it would have been of no avail at all for giving protection 

 against loss of the entire homologous chromosome and so the individual would 

 react in this case like one which had been haploid for that pair, just as the 

 data showed it did react. 



Still further evidence was advanced by Ostertag, and confirmed by Meyer, 

 that anoxia caused by a nitrogen atmosphere, when given as a post-treat- 

 ment to the irradiation over a period in which (if given by itself) it resulted 

 in little mortality, considerably accentuates the radiation-induced life-span 

 shortening. For this result is in accord with the known effect of anoxia in 

 hindering the restitution of broken chromosomes (Wolff and Luippold, 1955, 

 1956; Abrahamson, 1959). A similar pre-treatment with anoxia, on the other 

 hand, was found by Meyer to be ineffective. 



These conclusions may be applied to the interpretation of the differences 

 in X-ray-induced mortality found by those working with Hahrobracon of 

 different ploidy (Whiting and Bostian, 1931; Clark and KeUey, 1950; Clark 

 and Mitchell, 1951; Clark, 1957, 1960; Atwood et al, 1956), with Bombyx 

 of different ploidy (Tultseva and Astaurov, 1958), and with diverse 

 plants (e.g. Miintzing, 1941; Froier et al., 1941; Latarjet and Ephrussi, 1949; 

 Tobias, 1952; Mortimer, 1952, 1959). These authors had recognized their 

 results as evidence that the mortality, in effect a life-span shortening, was 

 genetic but it could not be concluded that the mechanism worked by way 

 of the loss of entire chromosomes. Similarly, in the work of Tsunewaki and 

 Heyne (1959a,b) on allohexaploid wheats, the greater vulnerability to 

 radiation of the types with one chromosome missing to begin with is seen to 

 be caused by a recessively acting genetic damage of some kind, which coidd 

 however be point-mutational, or regional deficiency, or whole chromosome 

 loss. 



On the other hand, when we turn to adult insects, with their non-dividing 

 ceUs and correspondingly far higher radiation resistance, how are we to 

 interpret Clark's recent (1960) result that, at all doses tried on adults, the 

 haploid still proves to be more vulnerable than the diploid? Possibly this is 

 a matter of point-mutations rather than chromosome loss, or the midgut 

 cells may still be dividing. But the enormously higher radiation resistance in 

 this case emphasizes the exceptional nature of the mechanism at work here. 

 In adult as well as young mammals, with their abundance of proliferating 

 tissues necessary for life, it must surely be the chromosome breaks that lie 

 at the basis of the radiation-induced life-shortening. 



